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Cells & Development @cellsdev.bsky.social · 25/09/2026

We heard through the vines that #cilia are hot (or not?) right now so here is a cool article by the Saxena lab about how Notch signalling inhibit zebrafish olfactory multiciliated cells differentiation 🐟 AND we got a cool movie with it too! #FluorescenceFriday www.sciencedirect.com/science/arti...

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Cells & Development @cellsdev.bsky.social · 25/09/2026

We're in love with our September issue cover! This stunning cover is from an article by the Rosin lab showing how CSF1R signaling impacts not only immune cells but also musculoskeletal development. Check out the article here: www.sciencedirect.com/science/arti...

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Cells & Development @cellsdev.bsky.social · 11/09/2026

Our latest published issue cover is here. From zebrafish 🐟 heart regeneration to deep learning based segmentation to insulin resistant. Check out our latest issue here: 👇👇👇 www.sciencedirect.com/journal/cell... #devbio

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Cells & Development @cellsdev.bsky.social · 04/09/2026

Vora and Rosin et al shows that CSF1R signalling is not only important in monocyte development but its in utero inhibition in 🐭 significantly affects cranioskeletal and muscle development, such as the mandible and the shape of their tongue. #devbio www.sciencedirect.com/science/arti...

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Cells & Development @cellsdev.bsky.social · 28/08/2026

A very intriguing story by Joao F. Botelho et al shows that in bird, the digit formation (their ✋) is not only governed by apoptosis but also due to changes in the rate of growth extension and cell division between the interdigital zone and the digital zone. So cool! #devbio doi.org/10.1016/j.cd...

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Cells & Development @cellsdev.bsky.social · 21/08/2026

Egfr is not the only signaling pathway important for stem cell development in Drosophila's testes. Judith Leatherman lab shows that Pvr/Pvf1 signaling also participates in cyst stem cells division, but its inhibition produces a distinct effect from Egfr in the testes. 👇👇👇 doi.org/10.1016/j.cd...

Fig. 1. Pvr and its ligand Pvf1 are expressed in the testis niche
Hub is marked with Fas3 stain and an asterisk in B, B’, with Fas3 and an arrow in C, C’, and with Ecad stain and an arrow in D, D’. Germ cells marked with Vasa (magenta in B–D). Cyst lineage cells marked with Tj (B). Bar in B = 10 uM. Architecture of the testis niche (A): the hub cells (blue) reside at the apex of the testis surrounded by germline stem cells (GSCs, light purple) and cyst stem cells (CySCs, light green). GSCs and CySCs divide to produce gonialblasts and cyst cells respectively. The gonialblast undergoes four mitotic TA divisions, guided by two cyst cells (dark green) which encapsulate them. Pvr (green in B, white in B’) accumulates in cyst lineage cells. Characteristic webbed stain that surrounds cysts of differentiating germ cells is typical of cyst cell membrane-localized stains. Pvf1 (green in C, white in C’) accumulates in the hub (arrow), colocalized with Fas3 (white in C). In Pvf1 lacZ enhancer trap line, β-gal (green in D, white in D’) accumulates in hub (arrow) colocalized with Ecadherin (white in D), and also in some late cyst cells (arrowheads).

Fig. 3. Cyst lineage expression of dominant negative (DN) Egfr or Pvr caused reduction in CySC numbers, fewer CySCs in S phase, and differentiation defects.

Fig. 5. Constitutively activated Egfr caused thinning of testes, while constitutively activated Pvr led to testis overgrowth and accumulation of early-stage cells.
Testes stained with Hoechst DNA dye (white), incubated at 29° for eight days. Bar in A = 50uM. Control (Tj Gal4; tub gal80ts) testes display brightest DNA stain in the niche region (asterisk) and in the coiled region of the seminal vesicle (A). λEgfr testes (Tj Gal4/UAS λEgfr; tub gal80ts) appeared thinner than control testes, consistent with loss of differentiating germ cells (B). Constitutive λPvr testes (Tj Gal4/λPvr; tub gal80ts) were enlarged compared to controls, and accumulated DNA-bright cells throughout the entire testis tube.

Fig. 6. Expression of constitutively activated Egfr or Pvr promoted loss of differentiating germ cells, while only Pvr promoted dramatic niche-independent proliferation of the cyst lineage cells.

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Cells & Development @cellsdev.bsky.social · 14/08/2026

Maternal protein restriction happens when pregnant mothers don't consume enough necessary dietary proteins required for fetal development. Pieter Vancamp et al found that this affects the global landscape of chromatin accessibility in the developing hypothalamus. Check it out doi.org/10.1016/j.cd...

Fig. 1. ATAC-seq analysis on fetal hypothalamic neural progenitors reveals ATAC-seq peaks enriched for TF binding sites. A: Schematic of the experimental design: Pregnant dams received a control (20% protein) or protein-restricted (PR: 8% protein) diet from gestational day (G) 0 to 17. Hypothalami were collected from four fetuses of each sex for each litter and pooled separately by sex. Following mechanical dissociation, cells were allowed to proliferate for 2 days to form neurospheres (NS), resulting in eight pools. A subset of each pool was used for RNA extraction serving RNA-seq and qPCR experiments (*one pool of NS from the PR group was unusable due to low RNA quality). Cells from fetuses of the same, from the two litters within each experimental group, were pooled. This resulted in four pools, which were used to generate independent libraries via ATAC-seq. B: Proportions of the differential ATAC-seq peak regions over the various genome annotations. C: Network visualization of genes associated with smaller ATAC-seq peaks in the PR group. Node color represents log₂ fold change (log₂FC); node size reflects centrality within the network, and edge thickness denotes interaction strength. Functionally related gene sets are grouped by shared GO terms, indicated by colored circles. D: Transcription factor binding motifs enriched in differential ATAC-seq peaks between Control (C) and PR groups. E: ATAC-seq peaks (BigWig and Bed files view in Integrative Genome Viewer or IGV) over the chromosome 20p12 genomic region encompassing the RT1-N1, RT1-S2, RTA-O1 and RT1-N3 genes.

Fig. 2. Correspondence between ATAC-seq peaks and gene expression. A: Position of differential ATAC-seq peaks relative to the Slc39a12, Fam111a and Nell2 genes (BigWig and Bed files view in IGV), and relative expression assessed by qRT-PCR in the neurosphere pools. B: Immunohistochemical staining for NELL2 on coronal sections of the G17 fetal rat brain, showing expression in both the hypothalamus (HT, white arrows) and cerebral cortex (CTX). Mapping of Nell2 on a feature plot of previously generated single-cell RNA-seq data of the G17 hypothalamus showed highest expression in neuroblasts. C: Position of differential ATAC-seq peaks relative to the Gabrb1 and Reln genes and feature plots from single-cell RNA-seq data highlighting the expression of the same genes in neuroblast and neuronal populations in the control condition (Vancamp et al., 2025).

Fig. 3. Identification of candidate RNA-seq genes reveals limited overlap with ATAC-seq peaks. A: Heatmap showing the 91 genes with different expression levels (nominal p value <0.05) between the neurosphere pools of the control (4 left columns) and PR groups (3 right columns). Black and red arrows indicate the genes that are further analyzed in the figure (D-E and F, respectively). B: Bar graph showing the significantly enriched GO terms associated with lower-expressed genes of the RNA-seq dataset. C: The Venn diagram shows the overlap between the 91 candidate genes identified by RNA-seq and genes associated with differential ATAC-seq peaks. D: Genome browser view of the RT1-A2 ATAC-seq peak. E: Genome browser view of the Zfp36 and Gsta4 gene ATAC-seq peaks overlapping the promoter region of the genes. Gene expression of the same genes assessed by RT-qPCR on the neurosphere pools. F: Mapping of selected genes on feature plots from single-cell RNA-seq data highlighting the expression of the Ccn1, Anxa2 and Gbp5 genes in the control condition in the G17 hypothalamus. Expression patterns reveal localization to specific cell types or restricted populations (highlighted by black arrows), pointing to potential functional relevance (Vancamp et al., 2025).

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Cells & Development @cellsdev.bsky.social · 07/08/2026

The testis is a fast evolving organ, and so is spermatogenesis. Did you know that bonobos have larger testicles than gorillas? In fact, they have the largest 🍒 in all of apes. Why? Well, @kaessmannlab.bsky.social et al discuss the molecular evolution of spermatogenesis here: doi.org/10.1016/j.cd...

Fig. 1. Major cell types in spermatogenesis. A segment of the cross section of a seminiferous tubule in the testes. In their development from spermatogonial stem cells to testicular spermatozoa, the cells move from the basal lamina of the seminiferous tubule towards the lumen, surrounded and nourished by Sertoli cells. The diploid spermatogonia differentiate into primary spermatocytes that undergo the first meiotic division, then called secondary spermatocytes, followed by the second meiotic division to form spermatids. These haploid cells differentiate from round spermatids to elongated spermatids and finally into immature spermatocytes, which detach from the Sertoli cells and travel to the epididymis, where they fully mature.

Fig. 2. Testicular chromatin remodeling. Throughout spermatogenesis (black arrow) histones are exchanged by testis specific histone variants. In the postmeiotic spermatids histones are exchanged by transition proteins (TNPs), the TNPs in turn are exchanged by protamines. The protamines facilitate the dense packaging of chromatin in the sperm head. During meiosis the unsynapsed sex chromosomes become sequestered in the sex body and transcriptionally silenced. One hallmark feature of the sex chromosomes in the sex body is the presence of phosphorylated H2AX along the entire chromosome length. Data from Kimmins and Sassone-Corsi (2005), and Turner (2015).

Fig. 3. Evolution of gene expression. Phylogenetic analyses of the translatome (thin and dark) and transcriptome (thick and light) for testis, liver, and brain (from top to bottom) reveal the rapid evolution of the testis. The branch lengths indicate evolutionary changes in expression levels. Data from Wang et al. (2020).

Fig. 4. Different rates of evolution in testicular cell types. Pairwise Spearman's rank correlation coefficient between human and other species for testicular cell types. The haploid cell types diverge faster than the diploid cell types. Adapted from Murat et al., Nature 2022, https://doi.org/10.1038/s41586-022-05547-7 | CC BY 4.0.

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Cells & Development @cellsdev.bsky.social · 31/07/2026

It is often said that cancer is like development gone wrong. One of the most important signalling pathways of development, the Wnt pathway, is frequently altered in colon cancer. Nydia Tejeda-Muñoz et al discussed the complex biology of Wnt signalling network. Check it out: doi.org/10.1016/j.cd...

Fig. 1. Central role of the Wnt pathway in tumor initiation and progression, and its crosstalk with major oncogenic pathways. Aberrant activation of the canonical Wnt/β-catenin signaling drives tumorigenesis by sustaining proliferative signaling, enforcing stem-cell–like programs, and promoting survival under oncogenic and therapeutic stress. The Wnt pathway output is further amplified through extensive crosstalk with key oncogenic modules, including PI3K/AKT/mTOR, RAS/RAF/MEK/ERK (MAPK), and TGF-β/Sma and Mad Related Proteins (SMAD), which integrate upstream mitogenic cues, metabolic states, and microenvironmental signals. These interconnected networks generate feedforward and compensatory feedback loops that enhance cellular plasticity, support epithelial–mesenchymal transition, and drive therapy resistance, intratumoral heterogeneity, and metastatic competence.

Fig. 2. RAS–RAF–MAPK and its interaction with β-catenin and PI3K–AKT–mTOR in colon cancer. Aberrant RAS–RAF–MEK–ERK activity modulates the canonical Wnt signaling through multiple mechanisms, including phosphorylation-dependent regulation of β-catenin stability, transcriptional enhancement of Wnt target genes, and MAPK-driven remodeling of the tumor microenvironment. Conversely, hyperactivation of Wnt/β-catenin can potentialize MAPK signaling by upregulating growth factor receptors, stabilizing RAS, and reinforcing downstream proliferative circuits. This reciprocal reinforcement establishes feedforward loops that promote tumor cell proliferation, stemness maintenance, EMT, and metastatic dissemination. In addition, MAPK inhibition frequently triggers compensatory reactivation of the Wnt signaling, underscoring their functional interdependence and highlighting the therapeutic relevance of dual-pathway targeting in RAS- or BRAF-mutated malignancies. Direct regulation is indicated in solid lines, indirect effects are indicated in dashed lines.

Fig. 3. Mechanistic integration of the Wnt/β-catenin pathway with the PI3K–AKT–mTOR pathway in cancer. The canonical Wnt activation modulates the PI3K–AKT–mTOR signaling through multiple nodes, including inhibition of GSK3β, stabilization of downstream effectors, and transcriptional induction of receptors and metabolic regulators that enhance PI3K pathway output. Reciprocally, PI3K–AKT signaling reinforces the Wnt/β-catenin activity by inhibiting GSK3β-mediated β-catenin degradation, promoting nuclear β-catenin accumulation, and facilitating the transcription of Wnt-dependent oncogenic programs. mTORC1 further integrates inputs from both pathways to regulate translational capacity, metabolic rewiring, and cancer stem cell maintenance. This bidirectional crosstalk creates feedforward loops that drive tumor growth, survival under stress, therapy resistance, and metabolic plasticity, underscoring the relevance of dual-pathway targeting in PI3K- and Wnt-driven malignancies. Direct regulation is indicated in solid lines, indirect effects are indicated in dashed lines.

Fig. 4. Role of the Wnt pathway in dorsal–ventral axis specification and maternal determinant relocation. The maternal Wnt/β-catenin signaling directs early dorsal–ventral axis formation in Xenopus early embryos. Cortical rotation after fertilization translocates maternal dorsal determinants, including Dishevelled (Dvl) and Wnt pathway activators, from the vegetal pole toward the future dorsal side (A). This asymmetric distribution inhibits GSK3β locally, stabilizes β-catenin, and activates dorsal-specific genes such as siamois and twin, establishing the dorsal organizer and early polarity (C). Without Wnt signaling, β-catenin is degraded, maintaining low cytoplasmic levels (B). Perturbations of this pathway produce distinct phenotypes: Wnt inhibition leads to ventralized embryos lacking dorsal structures, while Wnt hyperactivation causes dorsalization, expanded organizer activity, and axis duplication. Ectopic Wnt activation in ventral blastomeres can induce a secondary organizer, occasionally resulting in embryos with two heads.

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Cells & Development @cellsdev.bsky.social · 24/07/2026

Myelination of axons by Schwann cells (SCs) is a rather peculiar process. Degerny and Tawk et al show that there is a limited time window where SCs can myelinate, and this is linked to mitosis and Laminin expression. 🧠Check out the cool video and the publication here🧠: doi.org/10.1016/j.cd...

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Cells & Development @cellsdev.bsky.social · 17/07/2026

How does cells in a notochord pack together? And how packing affects the physical interactions between cells? Using physical modelling, Lubkin et al found a relationship between cellular packing and tension, pressure, and eccentricity. Check out the paper for more details: doi.org/10.1016/j.cd...

Fig. A1. Trigonometric relations used to estimate force balances and geometric ratios in (A) bamboo and (B, C) staircase patterns. Cells are modeled as spheres of radius R, clipped by planes. Angles at triple-junctions where cell pairs meet sheath are governed by force balances and determine geometric ratios of cells. Cell-cell interfaces: magenta; cell-sheath interfaces: teal; similar triangles yellow. A. Bamboo cells are modeled as radially symmetric barrel shapes, parallel to and sharing the notochord axis, with centroid-centroid distances h. B. Staircase cells are modeled as barrel shapes oriented parallel to the notochord axis, centered either left or right of the midline, and cut by the plane separating left and right sides of the notochord. C. For staircase, centroid-centroid distance h is half the cell height because of staggered arrangement. Similar triangles show that cos θ = c/R = h/R = 1/(1 + Γ). Limiting case occurs when θ = π/4, i.e. when , when cell-cell contacts become complete disks (dotted teal curve).

Fig. 1. A. 2D illustration of a 48 hpf zebrafish, showing anatomical position of notochord (magenta). B. Lowest-order regular cell patterns, “bamboo” (left) and “staircase” (right). Top: 2D schematic; bottom: 3D shapes of model pairs of interior vacuolated cells. Cell-cell boundaries (magenta) and sheath-cell boundaries (cyan) are modeled as single surfaces with respective surface tensions 2γc and γs+γc. C. A key nondimensional ratio is cells per unit length λ ≡ D/d, where d is the diameter of a sphere having volume V of a cell, and D is the diameter of a cylinder with the same volume V, whose height h is the centroid-centroid distance. D. Left: An ellipse with aspect ratio ⍺ defined as the ratio of the major (M) to minor (m) axis lengths. The eccentricity e of this ellipse is given by , assuming ⍺ ≥ 1. Right: Eccentricity e increases from 0 (circle) and approaches 1 (becoming flatter). E. Another key nondimensional ratio is Γ ≡ γs/γc, the ratio of sheath tension to inner cell tension. Unequal surface tensions at a cell-cell junction are shown in a force diagram. The contact angle θ satisfies the Young-Dupré equation (Schrader, 1995).

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Cells & Development @cellsdev.bsky.social · 10/07/2026

Heart injuries can often be fatal, yet many animals can regenerate their 🫀 without leaving any scar, while others like 👨 cannot. Part of the reason lies in how the extracellular matrix is regulated. Patra et al discussed in details how this works and what we can learn from 🐟 doi.org/10.1016/j.cd...

Fig. 1. Zebrafish heart development stages illustrated from 5 h to 5 days post-fertilization

Fig. 2. Schematic representation of the major extracellular matrix (ECM) components and their interactions during heart development.

Fig. 3. Schematic of ECM-associated congenital heart defects in zebrafish (Table 1 & 3). (A) Denotes the wild-type scenario. (B and C) Lack of med10 or med12 caused reduced cardiac jelly, impairing valve formation. Additionally, med12 deficiency causes trabeculation defects (Just et al., 2016; Segert et al., 2018). (D) npnta morphants exhibit an expanded AV canal with increased cardiac jelly in both atrium and ventricles, impaired trabeculation, and defective AVC valves (Patra et al., 2011). Orange arrows indicate the atrioventricular canal, red arrows indicate blood flow direction, hpf; hours post fertilization, dpf; days post fertilization, V; ventricle, A; atrium, OFT; outflow tract.

Fig. 4. Heart regeneration in adult zebrafish (Table 2 & 3). (A) Distinct stages of heart regeneration after cryoinjury in wild-type adult zebrafish. Injury triggers regenerative responses immediately after injury, beginning with blood clot deposition and neocoronary angiogenesis. Followed by CM proliferation and infiltration along the neocoronaries into the wound. Post-injury, during the 1st and 2nd week, collagenous scar gets deposited in the injured tissue. As the heart continues to regenerate, the fibrotic scar gradually regresses. The regeneration process is completed by 90-120 days post cryoinjury, marked with minimal or no scar remaining. (B) Disruption of hapln1-expressing epicardial cells or hapln1b mutation in zebrafish impairs cardiomyocyte proliferation and heart regeneration (J. Sun et al., 2022). (C) Fn loss-of-function zebrafish mutants exhibit poor regeneration following myocardial injury, attributed to impaired CM migration; however, CM proliferation remains unaffected (J. Wang et al., 2013). (D) In ccn2a-/- injured hearts, while angiogenesis was observed, CM proliferation and repopulation were disrupted (Mukherjee et al., 2020). dpci; days post cryoinjury, dpi; days post-injury, OFT; outflow tract, CM; cardiomyocyte.

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Cells & Development @cellsdev.bsky.social · 03/07/2026

In our Special Issue At the interface of Immunology and #devbio, Bellaïche et al discussed the surprising role of Toll-like Receptors in modulating tissue mechanics and tissue boundary segregation. We love it so much, we made an accompanied video of TLR7 😍 🔗: www.sciencedirect.com/science/arti...

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Cells & Development @cellsdev.bsky.social · 26/06/2026

Very curious study. I've always wondered how flatfishes 🐟have both their eyes on the same side. This is caused by the movement of one eye to other side of the skull, and this study by Bao et al suggests the role of autophagy in this movement! How interesting? Check it out: doi.org/10.1016/j.cd...

Observation of autophagy under transmission electron microscope. (A), autophagic vesicle (AV) in orbital tissue of the left eye. (B), autophagic vesicle in orbital tissue of the right eye.

Schematic drawing to explain the role of autophagy on eye migration in flatfish. (A), before the eye migration, cells located in the orbital tissue of both eyes begin to proliferate. Over proliferating cells in infraorbital tissue will generate an upward force as Bao's study had proved (Bao et al., 2011). Thus, the tissues surrounding both eyes will suffer varying degrees of mechanic force, which might cause different degrees of autophagy. Compared with the infraorbital tissue, more autophagy happens in the supraorbital tissue; and compared with the stationary eye, more autophagy takes place around the mobile eye. Once the eye on blindside receives sufficient push force from the infraorbital tissue to overcome the counteracting force from the supraorbital area, it would migrate upwards. (B), the counteracting force grows larger as the two eyes get closer. Meanwhile, the autophagy around the eyes especially the mobile eye becomes more and more intense. (C), when the migrating eye reaches the place where the push force and counteracting force get balanced, it finally stops, and the autophagy around the eyes decreases.

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Cells & Development @cellsdev.bsky.social · 19/06/2026

This is SO cool! Ever wondered how our stomach has that left-leaning pouch shape? All stomach started out as a symmetrical tube, yet as the organ develops, it curves to one side. By using modelling, Lubkin et al shows the curve is caused by the thinning of the left side! doi.org/10.1016/j.cd...

Fig. 1. Vertebrate embryonic stomach bending in vivo. A. The initially straight foregut tube is illustrated from the esophagus (esoph) to the proximal intestine (duodenum, duod), and divided into left (light blue) and right (dark blue) halves. During bending, the stomach region (stom) curves leftward, forming a concavity on the right and a convexity on the left. Simultaneously, the left stomach lengthens in the longitudinal direction (z). B. Transverse cross sections (dotted lines in A) through the stomach of the Xenopus laevis embryo (anterior view) show that, during bending, the left wall of the stomach (light blue) also expands in the circumferential (θ) direction and thins in the radial (r) direction, while the right wall (dark blue) flattens and subsequently becomes concave. Embryonic staging is according to Nieuwkoop and Faber (NF; (Zahn et al., 2022)) Anterior (A), posterior (P), dorsal (D), ventral (V), left (L) and right (R) orientations are as indicated.

Fig. 3. Growth and differential growth of a simple tube. A. Initially symmetric tube, in perspective and cross-section. Intrinsic growth of the left and right sides can be considered separately, and experimentally observed by cuts. B-E Labeling (yellow boxes): +/−/0 designates left stretch ratio greater than/less than/equal to right stretch ratio in the same direction. B. Both sides grow isotropically by the same amount (homogeneous growth). and are equal and equal on left and right, so there is a change in size (from A) but not shape. C. Volumetric growth of both left and right sides is isotropic, but unequal (inhomogeneous). and are greater on the left than the right, so tissue volumes do not remain equal. D. Volumetric growth in only one direction. If tissue grows faster in one direction but the same in the other (anisotropic growth, e.g., by oriented cell divisions), its stretch ratios and are unequal. Here right and and left are equal, but left is greater, so volumetric growth is greater on the left than the right. E. Volume-conserving growth on both sides. Anisotropic growth that preserves volume (e.g., by cell rearrangement) must balance elongation in one direction with shrinkage in another direction. is smaller on the left than on the right, and is greater on the left than on the right. F–I Stress induced by growth. First principal stress (positive, tension, blue; negative, compression, red) shown in arbitrary units below their corresponding ‘cut’ schematics. F. Homogeneous growth does not create shape change or residual stress. C, D, E. Differential growth leads to incompatibility of left and right shapes, which no longer fit without additional modification. Internal (residual) stresses must be generated to bend and stretch tissue, to maintain tissue continuity across the LR boundary (G, H, I).

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Cells & Development @cellsdev.bsky.social · 18/06/2026

Excellent news: The latest figure shows that our impact factor has risen to 2.5. This takes an incredible amount of work, from how papers were selected, to how they were perceived by scientists in the field. We covers topics in cells, #devbio, 🌱or animals, biomechanics, and more. @isdb.bsky.social

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Cells & Development @cellsdev.bsky.social · 12/06/2026

Cancer progression and formation is similar to many developmental processes. It is unsurprising that many genes are shared between these two processes, and one of which is BRCA1. BRCA1 regulates cell cycle and genome integrity during development. Check out the latest review: doi.org/10.1016/j.cd...

Fig. 1. Conserved BRCA1 protein structure between species. Key domains and regions in the BRCA1 protein in the indicated species are shown, including Really Interesting New Gene (RING) finger domain, BRCA1 C-terminus (BRCT) domain 1 and 2, Partner and Localizer of BRCA2 (PALB2) interaction domain, and disordered regions. Note that the domains and regions are highly conserved in primates, non-primate mammals, vertebrates, and invertebrates.

Fig. 2. Functions and mechanisms of BRCA1 in early embryo development. (Top left) Genome integrity. During early development, embryos are subject to genomic instability from diverse sources, including replication-derived or transcription-derived (R-loops) stress, oxidative stress, and parentally inherited damage. BRCA1 is involved in the prevention and repair of genomic damage mediated by homologous recombination (HR). (Top right) Cell proliferation. Early embryos undergo rapid cleavage divisions and incur extraordinary proliferative demands. BRCA1 is involved in successful proliferation and germ layer formation, particularly through activation of the p53 checkpoint pathway. (Bottom left) Chromatin remodeling. In early embryos, BRCA1, in concert with BARD1, plays a role in suppressing transcriptional initiation. By altering the acetylation (Ac) of histones H4K8, independent of its established H2A activity, BRCA1-BARD1 alters recruitment of chromatin reader BRD4. (Bottom right) Transcription. As the early embryo approaches zygotic genome activation (ZGA), transcriptional demands exponentially increase. BRCA1 directly interacts with transcription factors (TFs), transcriptional repressors, and RNA Polymerase II (Pol II), and therefore likely plays a shaping role in the early transcriptional environment. Abbreviations: BRCA1, Breast Cancer gene 1; HR, homologous recombination; BARD1, BRCA1 Associated RING Domain 1; BRD4, Bromodomain-containing protein 4; Ac, acetylation; Pol II, RNA Polymerase II.

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Cells & Development @cellsdev.bsky.social · 05/06/2026

In this beautifully illustrated review, Carmen Ruiz de Almodóvar et al discuss the relationship between the vasculature network and neurogenesis in the subventricular zone (SVZ) and the subgranular zone (SGZ). It turns out that this is a 2-way communication interaction. doi.org/10.1016/j.cd...

Fig. 1. The SVZ neurogenic niche and its vasculature.
(A) Schematic illustration of the subventricular zone (SVZ) neurogenic niche in the adult mouse brain depicting cellular and molecular components. Neural stem cells (NSCs; type B cells) generate transit-amplifying cells (type C cells), which in turn give rise to the migrating neuroblasts (type A cells). NSCs are located beneath the ependymal cells which line the cerebrospinal fluid (CSF)-filled lateral ventricle. They have a polarized morphology, with a long basal process to contact the vasculature and a small apical process that harbors a primary cilium and extends through the ependymal cell layer to directly access the CSF. In addition to the aforementioned cell types, astrocytes and microglia contribute to the cellular architecture of the niche. (B) Both the choroid plexus and the vasculature provide signals that are important for the regulation of NSCs and their progeny.

(A) Schematic illustration of the subgranular zone (SGZ) neurogenic niche in the adult mouse brain. Radial glial like cells (RGLs) give rise to intermediate progenitor cells (IPCs) which produce migrating neuroblasts (NB). NB migrate to the granular cell layer of the hippocampus where they differentiate into granule cells. The radial processes of RGLs interact with ECs of blood vessels in regions lacking a basement membrane. Note that IPCs and NB also interact with blood vessels. Moreover, pericytes and astrocytes envelop vessels surface making up what is termed neurovascular unit (NVU). (B) Molecular mechanisms described in the communication between neural progenitors and blood vessels in the SGZ. Different categories have been established according with the biological process in which they are involved.

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Cells & Development @cellsdev.bsky.social · 29/05/2026

#Devbio is fascinating because what do you mean we can learn about stem cell biology and aging by studying a tiny minimalistic creature like the Hydra? 🤯 In this fascinating review, Thomas W. Holstein discussed how the Hydra can be used as a model system for these processes. doi.org/10.1016/j.cd...

Living budless polyp illustrating the distribution of the interstitial stem cell lineage and gastric neurons in Hydra. The founder polyps of this cross were a Hym-176B::GFP (Noro et al., 2021)(green) and a Nanos::RFP transgene (Nishimiya-Fujisawa and Kobayashi, 2018)(magenta). Hym-176B::GFP neurons represent a peptidergic neuron subset in the gastric region, which was described before (Noro et al., 2019), and which is involved in the longitudinal contractions of the polyp's ectoderm and which corresponds to the CB circuit (Dupre and Yuste, 2017; Noro et al., 2021). The lineage was generated by Hendrik Petersen and Chiemi Nishiyama-Fujisawa in our lab. Images of living polyps were taken by Ulrike Engel (COS, Nikon Imaging Center).

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Cells & Development @cellsdev.bsky.social · 22/05/2026

During morphogenesis, different tissue interacts with one another, either mechanically or biochemically. Patrick P.L. Tam and Pragathi Masamsett show that the anterior mesendoderm can pattern head formation in mouse embryos by regulating WNT signalling. Check it out here: doi.org/10.1016/j.cd...

Fig. 1. Contribution of cell populations that possess axis inducing activity, early gastrula organizer, the mid-gastrula organizer and the node of the gastrulating mouse embryo, to the axial mesendoderm of the early-somite stage embryo.

Fig. 2. Anteriorization of the epiblast. (A) Regionalization of signalling activity across the anterior-posterior dimension of the gastrulating embryo. Left: early-streak stage; right: late-streak stage. (B) Regionalization of the germ layer precursors in the epiblast showing the ectoderm precursor localized to the domain of low WNT, Nodal and BMP signalling activity. Left: early-streak stage; right: late-streak stage. (C) Epiblast stem cells, derived from the epiblast of early-streak embryo under different signalling conditions, mapped to developmentally equivalent cell populations in the epiblast and primitive streak. Signalling molecules: FGF2, fibroblast growth factor 2; Activin, Activin A; signalling inhibitors: IWP2, WNT inhibitor; SB: SB431542 TGFβ/Smad inhibitor. The location of epiblast stem cells with different lineage propensity is displayed in the corn plot of the epiblast and primitive streak, with the position defined by coordinates in the distal (1)-proximal (11) dimension, and anterior (A)-(left (L)-right (R)-posterior (P) domains in the transverse plane; relative preponderance of the cell types at each position indicated by the colour scale.

Fig. 3. Genetic activity in the visceral endoderm and anterior mesendoderm. (A) Genes expressed in the anterior visceral endoderm including those encoding antagonists of WNT and Nodal signalling. (B) Genes expressed in the anterior mesendoderm, encompassing those that encode antagonists of WNT and BMP signalling. (C) Foxa2-Otx2-Lhx1 regulate the expression of genes encoding WNT antagonist and factors that modulate WNT signalling activity. Solid connector, direct action; dash connector, indirect action. Left panel: Expression of Lhx1 in the anterior mesendoderm (arrow). Right panel: Expression of Tcf-LacZ reports the pattern of WNT signalling activity, showing low WNT activity in the anterior region of the late-streak embryo.

Fig. 4. Functional attribute of the anterior mesendoderm in modulating WNT signalling activity for pattering the embryonic brain. (A) Graded pattern of WNT signalling activity in the anterior-posterior dimension of (i) the early-bud (E7.25) embryo, (ii) head folds of early-somite (E8.5) embryo and (iii) brain of early-organogenesis (E9.5) embryo. Area of high WNT signalling activity, highlighted by the expression of the Tcf-LacZ reporter and shown as green region in the schematics. * Regions of low WNT activity in the epiblast, head folds and embryonic brain. A, anterior; P, posterior; fb, forebrain; mb, midbrain; hb, hindbrain. (B) Mutant Dkk1−/−, Lrp6Gw/Gw and Ctnnb1bf/bf embryos showing escalated WNT activity (Tcf-LacZ reporter expression) and phenocopy of head truncation (arrow). (C) Increasing severity of head truncation (II to V) with progressive loss of rostral brain structures associated with diminishing antagonistic activity and escalating WNT activity in mutant embryos (I: Dkk1+/−, Lrp6gw/+ and Ctnnb1bf/+; II: Lrp6gw/+;Ctnnb1bf/+, III IV: Lrp6gw/gw, Ctnnb1bf/bf, Dkk1+/−;Lrp6gw/+, and Dkk1+/−;Ctnnb1bf/+, V: Dkk1+/−; Lrp6gw/+; Ctnnb1bf/+, Fossat et al., 2011). A, anterior; P, posterior; t, telencephalon; d, diencephalon; m, myelencephalon. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

0117

Cells & Development @cellsdev.bsky.social · 15/05/2026

How to make a ❤️ in a dish? This very comprehensive review from the lab of Gergana Dobreva discusses everything you need to know, from the chemical signalling to mechanical signalling that governs cardiogenesis, to the current protocols of how to make this organ in vitro. doi.org/10.1016/j.cd...

Fig. 1. Signalling pathways controlling first and second heart field development. A. Schematic representation of the contribution of the first heart field (FHF) and second heart field (SHF) during mouse embryonic heart development. B. Major signalling pathways known to control the specification, proliferation and progressive differentiation of FHF and SHF progenitor cells in the developing heart.

Fig. 2. Summary of cardiomyocyte differentiation protocols. A. Cardiomyocyte differentiation through regulation of Nodal/Activin A and BMP signalling (Kattman et al., 2011). B. Generation of atrial and ventricular cardiomyocytes through activation or inhibition of RA signalling (Zhang et al., 2011). C. SAN-like pacemaker cell differentiation form hESCs through modulation of BMP and RA signalling (Protze et al., 2017). IWP-2: Wnt Inhibitor; SB: TGFβ inhibitor SB-431542. D. Chemically defined generation of human cardiomyocytes from hPSCs (Burridge et al., 2014). The figure was designed with BioRender.

Fig. 3. Cardiac organoids. A. Schematic representation of the protocol for generation of hPSCs-derived heart-forming organoids (HFOs) (Adapted from Drakhlis et al., 2021a). B. Schematic representation of the protocol for generation of self-assembling human vascularized heart organoids developed by Lewis-Israeli et al., 2021. C. Schematic representation of the protocol for generation of hPSCs-derived cardioids developed by Hofbauer et al., 2021. The figure was designed with BioRender.

Fig. 4. Heart-on-chip and organ-on-chip devices. A. 3D heart on chip device, used to drive cardiac maturation via mechanical stimulation, reproduced from Marsano et al., 2016 with permission from The Royal Society of Chemistry under STM Guidelines on Permissions. B. 3D Biowire II-heart-polystyrene-chip-model, used to mature cardiomyocytes via electrical stimulation and to examine the optimal conditions for cardiac tissue engineering, reproduced from Zhao et al., 2020 with permission from Elsevier under STM Guidelines on Permissions. C. 3D heart-on-chip device, used for monitoring of biophysical parameters of engineered heart tissues, reproduced from Zhang et al., 2021 with permission from Elsevier under STM Guidelines on Permissions. D. Cardiac-fibrosis-on-a-chip model with hallmarks of fibrosis-induced heart failure, reproduced from Mastikhina et al., 2020 with permission from Elsevier under STM Guidelines on Permissions. E. Organ-on-a-chip model for testing anti-tumour effects and cardiotoxicity, reproduced from Chramiec et al., 2020 with permission from Copyright Clearance Center, Inc. (“CCC”) under STM Guidelines on Permissions.

0113

Cells & Development @cellsdev.bsky.social · 08/05/2026

Can't quite say we've seen many papers studying 🦷 #development. In this curious paper, Sun et al shows a double negative loop between a long non-coding RNA (LOC102159588) and a microRNA (miR-133b) is important for apoptosis regulation and normal 🦷 development in mice. doi.org/10.1016/j.cd...

Mechanistically, miR-133b repressed the transcription of LOC102159588 through downstream target Sp1. Conversely, LOC102159588 not only inhibited the transport of pre-miR-133b from the nucleus to the cytoplasm by regulating exportin-5 but also served as a sponge in the cytoplasm, suppressing functional miR-133b. Together, the double-negative feedback loop maintained normal tooth morphogenesis by modulating endogenous apoptosis. Related disruptions would lead to an arrest of tooth development and may result in tooth malformations.

Fig. 4. LOC102159588-miR-133b axis regulated tooth morphogenesis via endogenous apoptosis. (A) Schematic illustration of the experimental procedure. (B) Morphological characteristics and three-dimensional reconstruction of tooth. Scale bar = 1 mm. (C) Quantification analyses of volume of enamel and detin. (D) Quantification analyses of Mineral density. n.s., not significant.

074

Cells & Development @cellsdev.bsky.social · 01/05/2026

Do you work with #zebrafish? Wanting a budget-friendly housing system capable of thermal control and filtration? Perhaps you just set up your lab and are looking for a short term solution? Then ZebRack designed by the Valdivia lab might pique of your interest? Check it out: doi.org/10.1016/j.cd...

Fig. 1. The ZebRack housing system. (A) Frontal view of the ZebRack setup at the Universidad Mayor fish facility. With a capacity for 15 Aquaneering 2.8 L tanks, its lightweight and compact frame can house up to 225 adult zebrafish (at a maximum of 15 fish per tank). (B) Rear view of the ZebRack, illustrating the water flow system designed in OnShape. Blue arrows indicate water flow from the reservoir to the fish tanks. Drainage water then flows back to the reservoir (yellow arrows), where it passes through an external filter for cleaning before being recirculated.

Fig. 2. Water reservoir and external filter (view from above). A submersible pump transports water from the reservoir up to the fish tanks. Drainage water then returns to the reservoir, where it is purified by the external filter. This filter, connected to the reservoir, features its own UV light, prefilter pads, activated charcoal, and ceramic bio-rings to maintain water quality.

Fig. 3. ZebRack setup at the 2025 International Developmental Biology course. (A) The ZebRack system during a course in Quintay. The two upper levels were used for fish tanks, while the lower level was dedicated to breeding boxes. The entire apparatus was housed within a portable indoor culture tent alongside a portable AC unit. The tent was fully closed at night to ensure temperature stability. (B) A close-up view of the interior of the indoor tent.

0105

Cells & Development @cellsdev.bsky.social · 24/04/2026

Neurulation is mechanically expensive where shape and positional changes of the cell sheet take place. Using a vertex model, @fzolessi.bsky.social shows that it is the relative difference in surface tension between apical-basal vs lateral side that controls this process. doi.org/10.1016/j.cd...

094

Cells & Development @cellsdev.bsky.social · 17/04/2026

An interesting paper from the Kojic lab shows that ankrd1a - a stress responsive gene is consistently unregulated near damaged site in the ❤️ in zebrafish. Loss of ankrd1a leads to an increase in dedifferentiating cells. Check it out here: doi.org/10.1016/j.cd...

Fig. 1. Early expression of TgBAC(ankrd1a:EGFP) transgene in the border zone CMs. Hearts of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) (n = 4) were cryoinjured and left to recover for 6 and 15 h. White dashed line outlines the ventricle. Scale bars, 200 μm.

Fig. 6. Persistent TgBAC(ankrd1a:EGFP) expression in CMs adjacent to the residual scar. Hearts (n = 4) of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) zebrafish were cryoinjured and analyzed at 30 dpci, showing different levels of scar resolution (least (A) to most (D) regenerated). The whole hearts after dissection were imaged by fluorescence microscopy (A-D). Serial sections were used for AFOG staining (bright-field images on panels А'-D′) and fluorescence imaging by confocal microscopy (А"-D″). In the indicated region of injury on panels A'-D′, collagen is stained blue, fibrin is stained orange, and CMs are stained brown. Scale bar, 100 μm.

1139

Cells & Development @cellsdev.bsky.social · 03/04/2026

An interesting paper from the lab of Edgar Krötzsch showing the potential contribution of tissue-resident macrophages in the regeneration of punched holes in mouse's ear. Depleting macrophages with clodronate liposomes reduced regeneration and induced cartilage formation. doi.org/10.1016/j.cd...

052

Cells & Development @cellsdev.bsky.social · 27/03/2026

Some say development is guided by forces. While the role of chemistry in dev bio is undeniable, growing evidence has pointed out the significant contribution of physics too. Chowdhury et al discuss how forces shape normal and cancer stem cells and the clinical applications. doi.org/10.1016/j.cd...

Fig. 1. Force impact on embryogenesis and organogenesis. Compelling evidence from published reports demonstrates that fate and differentiation of embryonic stem cells and adult stem cells depend on forces (shear and/or normal stress), substrate elasticity/viscoelasticity, and substrate topography. The observation from cell culture studies that mesenchymal stem cells undergo neurogenesis on soft substrates is consistent with the finding that a stiffness gradient is responsible for axons to change their turning direction caudally towards soft tissues in the developing Xenopus embryonic brain in vivo. Stem-cell based models are useful in understanding role of forces in the development of embryos, which are inaccessible in vivo for mammalian embryos. Blastoid formation via iPSCs is enhanced by 3D culture and substrate mechanics and may depend on endogenous forces (endo-force). Maturation of cardiomyocytes from iPSC differentiation is promoted by mechanical stretching. iPSC, induced pluripotent stem cells. Force is used here generically to represent any type of mechanical loading (force, torque, tensile or compressive stress, shear stress, torque per volume or specific torque) (exogenously or endogenously).

Fig. 2. A mechanobiology model of tumor cell self-renewal and metastasis. Matrix metalloproteinases (MMPs) from the primary tumor site soften the extracellular matrix (ECM) of the tumor microenvironment and break tumor cell dormancy, leading to tumor cell invasion. Stiff (>800 Pa) differentiated tumor cells and soft (<300 Pa) undifferentiated tumor stem cells such as tumor-repopulating cells (Lv et al., 2020) enter blood vessels (intravasation), arrest at narrow vessels, and exit blood vessels (extravasation) to metastasize to distance sites and form micrometastasis. In some cases, soft tumor stem cells proliferate and self-renew within a soft matrix (e.g., bone marrow, brain, lung, and liver) to establish metastatic colonization and grow into macroscopic metastases, or survive and enter dormancy within the stiff matrix, whereas stiff differentiated tumor cells die in the soft or stiff matrix of a different tissue (denoted by an X). In some other cases, when the matrix of tumor microenvironment of metastatic sites becomes inflamed and then softened, soft dormant tumor stem cells will exit dormancy, self-renew, and grow into clinically-detectable macroscopic metastases. Note that this simple model illustrates an element of the Virchow's postulate and highlights softness-based mechanoregulation of cancer progression, which is also regulated by other physical and soluble factors and cells such as tumor-associated fibroblasts and immune cells.

Fig. 3. Cell softness regulates cytotoxic T cell killing of tumor cells. Cytotoxic T cells enter tumor parenchyma, where the T cells use T cell receptor (TCR) to recognize MHC (major histocompatibility complex)-tumor antigenic peptide complex and form the synapse. The activated T cells then release perforin and granzymes to the synapse space where perforin forms pores on the plasma membrane of target tumor cells and allows the entry of granzymes into the cytoplasm, activating caspases 3 and 7 and leading to tumor cell apoptosis. However, drilling pores by perforin is not only a chemical but also a mechanical process. Cell stiffness (>600 Pa) is required for the pore formation by perforin and cell softness impairs perforin pore formation. Thus, soft (<300 Pa) tumor stem cells such as tumor-repopulating cells use their softness to evade T cell cytolysis by impeding perforin pore formation. On the other hand, activated T cells might be very soft, avoiding autolysis. In addition, it is possible that TCR-MHC binding may be equal in the molecular number but the interacting force may be weaker between the soft tumor cell and the immune cell than between the stiff tumor cell and the immune cell; as a result, the released granzyme and perforin from the immune cell may be less, contributing to less killing of the soft tumor cell. Stiff target cells are engulfed more avidly than soft target cells by macrophages, suggesting that this model may be applied to other immune cells.

0138

Cells & Development @cellsdev.bsky.social · 20/03/2026

Many ion channels eg. TRP, Piezo are mechanically sensitive, meaning they can be activated/deactivated by mechanical stimuli such as membrane curvature or substrate stiffness. In this thorough review from the Mayor lab, they discuss how these channels regulate cell migration. doi.org/10.1016/j.cd...

Fig. 1. Basic steps of cell migration. (a) Mesenchymal cell migration. Cells are attached to the extracellular matrix (ECM) via integrins and focal adhesions (FA). Actin polymerization at the leading edge extends filamentous actin (F-actin) protrusions inducing a front-rear polarization. New FA adhesions attach the protrusions to the ECM followed by F-actin rearward movement, known as actin retrograde flow. Disassembly of rear FA and myosin II contraction at the back of cell generate the pushing force to move the cell forward. (b) Amoeboid cell migration. Cells do not form adhesions with the ECM or other cells. Under confinement, amoeboid cells form membrane blebs, also known as pseudopodia, inducing a front-rear polarization. Actin retrograde flow is initiated by mechanical forces, such as confinement. Myosin II contraction at the back of cell generates the pushing force to move the cell forward.

Fig. 2. MS ion channel families involved in cell migration. (a) Transient receptor potential channels (TRP). TRP channels form 6 transmembrane (TM) domains. TM 1-2 are represented in cyan, TM 3-4 in orange and TM 5-6 in magenta. The pore forming domain is formed between TM5 and TM6. Each subfamily of TRP channels contains unique domains in the cytoplasmic N- and C- termini. TRPC channels have three ankyrin repeats and a coiled-coil domain in the N-terminus. A TRP domain, which has gating functions, a calmodulin and IP3R binding domains are localized in the C-terminus. TRPV channels have six ankyrin repeats in the N-terminus. A TRP domain, a calmodulin and PIP2 binding domains are localized in the C-terminus. (b–b′) Piezo1 channels. (b) Each Piezo1 channel has at least 26 TM regions and up to 40 TM domains. The TM domains form three defined structures, known as blades. Each blade is colour coded in cyan, orange and magenta for easier representation. The carboy-terminal extracellular domain (CED) is located directly on top of the pore forming domain and is important for ion selectivity (Zhao et al., 2016). (b′) Due to its large size, a Piezo1 channel induces a small curvature to the plasma membrane, when force is applied the plasma membrane is stretched, thereby opening the Piezo1 channel.

Fig. 3. Role of MS ion channels in cell migration. (a) Actin protrusions. MS ion channels can regulate the extension of actin-based protrusions through PI3K signalling. Ca2+ binding to PI3K leads to the activation of several Rac1-GEFs, including P-Rex1 and SWAP-70, Vav1, Sos1. Rac1-GEFs mediate the transition from inactive Rac1-GDP to Rac1-GTP, leading to actin polymerization and protrusion extension. (b) RhoA activation. The Ca2+ sensitive Pyk2 kinase is activated after MS ion channel opening. Pyk2 activates PDZ-RhoGEF which mediates the transition from inactive Rho-GDP to Rho-GTP, leading to Myosin II phosphorylation. Global Myosin II contraction leads to inhibition of cell migration. (c) Chemotaxis. The presence of a chemoattractant agent leads to re-localization of TRPC1 and TRPC6 MS ion channels to the direction of the chemoattractant signal. Localized Ca2+ can regulate actin remodelling via PI3K or induce Ca2+ flickers at the leading edge of the cell, promoting directional cell migration. (d) Focal adhesion (FA) disassembly. MS ion channels regulate FA disassembly via calpain, a Ca2+ dependant protease that mediates FA degradation. Restricted calpain activity at the rear of the cell mediates specific FA disassembly at the back of the cell, promoting cell migration. (e) Yap/Taz nuclear localization. Piezo1 activation is correlated with Yap translocation from the cytoplasm to the nucleus, leading to Yap mediated gene transcription. However, the biochemical signals downstream of Piezo1 have not been identified yet. Dashed line represents unknown signalling proteins.

01310

Cells & Development @cellsdev.bsky.social · 13/03/2026

Negative results are just as important as positive ones. They inform future investigations of what to focus on, saving resources. In this study, Wang et al showed that the protein LSM14A is dispensable for spermatogenesis and male fertility in mice. Check it out: doi.org/10.1016/j.cd...

Fig. 2. Generation and validation of Lsm14a conditional knockout mice.
(A) Lsm14a targeting strategy: loxP sites (arrowheads) flank exon 2. Germ cell-specific knockout mice were generated by crossing Lsm14aflox/flox mice with Stra8-Cre mice. (B) Genotyping profiles: Wild-type (WT) allele (198 bp), floxed allele (260 bp), Cre-mediated deletion (174 bp). Genomic DNA from Stra8-Cre mice exhibits both the WT (702 bp) and Cre-recombined (400 bp) bands. (C) RT-qPCR analysis of Lsm14a mRNA levels in adult control and Lsm14a cKO testes. Gapdh serves as loading control (n = 3). (D-E) Western blot analysis of LSM14A protein expression in testicular lysates. Band intensities were normalized to GAPDH (loading control). Quantitative data shown in panel E (n = 4). (F) Immunofluorescence of P19 testicular sections. Right panels show magnified boxed regions. Dashed lines demarcate spermatocyte clusters; arrows indicate representative spermatocytes. LSM14A signals (red) are absent in Lsm14a cKO spermatocytes. SYCP3 (green) marks synaptonemal complexes; nuclei counterstained with DAPI (blue). Scale bars = 20 μm. (G-H) Morphological and gravimetric comparisons of adult control and Lsm14a cKO testes/epididymides. All data are presented as mean ± SEM. Statistical significance was determined by two-tailed Student's t-test: ns (not significant), ****P < 0.0001.

Fig. 3. Lsm14a deficiency does not impair spermatogonial differentiation or meiotic development of spermatocytes.
(A) Immunofluorescence of adult testicular sections co-stained with DDX4 (red, germ cells), PLZF (green, undifferentiated spermatogonia), and DAPI (blue, nuclei). Scale bar = 40 μm. (B) Quantitative analysis of PLZF+ cells per seminiferous tubule cross-section from panel A. (C) Testicular sections co-stained with DDX4 (red), c-KIT (green, differentiated spermatogonia), and DAPI (blue). Scale bar = 40 μm. (D) Quantification of c-KIT+ germ cells per tubule from panel C. (E) Germ cell marker co-localization: DDX4 (red), SYCP3 (green, meiotic spermatocytes), DAPI (blue). Scale bar = 40 μm. (F) SYCP3+ spermatocyte counts per tubule from panel E. (G) Meiotic chromosome spreads stained with γH2AX (red, DNA damage foci) and SYCP3 (green, synaptonemal complexes). Scale bar = 5 μm. (H) Stage-specific quantification of meiotic cells from panel G. More than 600 cells were counted in each experiment (n = 3). (I) Testicular niche visualization: WT1 (red, Sertoli cells), DDX4 (green), DAPI (blue). Scale bar = 40 μm. (J) DDX4+ germ cell quantification per tubule from panel I. All data are presented as mean ± SEM. Statistical significance was determined using a two-tailed Student's t-test: ns (not significant).

Fig. 4. Lsm14a deficiency does not affect haploid germ cell development, morphogenesis, or acrosome formation.
(A) Periodic acid-Schiff (PAS)-stained adult testicular sections depicting seminiferous tubules at stages I-XII, with developing germ cell populations. Lower panels show magnified boxed regions. Scale bars = 40 μm. Abbreviations: PL, preleptotene spermatocytes; L, leptotene; Z, zygotene; P, pachytene; Di, diplotene; M, metaphase; S1–16, haploid spermatids at steps 1–16. (B) Immunofluorescence of testicular sections co-stained with SYCP3 (red, meiotic marker), peanut agglutinin (PNA, green, acrosomal marker), and DAPI (blue, nuclei). Seminiferous tubules at stages I-XII are shown, with lower panels providing magnified views of boxed regions. Scale bars = 40 μm.

083

Cells & Development @cellsdev.bsky.social · 13/03/2026

Our cover image for the March issue is up! Check out the issue here: www.sciencedirect.com/journal/cell...

052

Cells & Development @cellsdev.bsky.social · 06/03/2026

Two complementary articles from the lab of Anming Meng and Katie McDole discussing the history and biology of organizer in 🐟, 🐸, and 🐭. Even after more than 100 years since its discovery, major questions remain, especially for mammals. doi.org/10.1016/j.cd... doi.org/10.1016/j.cd...

02713

Cells & Development @cellsdev.bsky.social · 27/02/2026

Neurogenesis, as turns out, is highly dependent on cytokine signalings. Even more interesting, the landscape of cytokines in the CNS is highly localised, and a large proportion of cytokine production is done by the meninges. This review by Rua et al discusses in more detail: doi.org/10.1016/j.cd...

0134

Cells & Development @cellsdev.bsky.social · 20/02/2026

The importance of epigenetic modifications in embryonic development has been cemented. In mammals, the trophoblasts play a crucial role in implantation, and their DNA methylation status is crucial. This detailed review by Hua Zhang et al discussed just how important this is: doi.org/10.1016/j.cd...

Fig. 1. An epigenetic roadmap for early trophoblast development in mice. The trophoblast lineage exhibits lower levels of DNA methylation compared to the embryonic lineage. At the late 2-cell stage, Carm1 expression increases to varying degrees in each blastomere. The high level of Carm1 biases the fate of ICM. As early as the 4-cell stage, all blastomeres initiate an imprinted XCI, which is controlled by maternal H3K27me3 imprinting on the Xist gene. At the 8–16-cell stage, high levels of the chromatin remodeling protein Smarcc1 in partial blastomeres at the late 8-cell stage upregulate epithelial keratins to determine the fate of the trophectoderm. Imprints of placental origin, mediated by the LncRNA Kcnq1ot1, are established during the process of trophoblast lineage differentiation between E4.5 and E7.5. Furthermore, chromatin-modifying enzymes play important roles in post-implantation trophoblast differentiation. ICM, inner cell mass; XCI, chromosome inactivation.

Fig. 4. Chromatin-modifying enzymes and their essential roles in embryonic/fetal development in mice. (A). Null mutations of chromatin-modifying enzymes can lead to embryonic or fetal development failure at various stages. The blue genes are genes that play a role in cell survival. The red genes are genes that play a role in trophoblast development. (B). The phenotypes of placental development defects resulting from mutations in chromatin-modifying enzymes. DNA methylation and histone modifications regulate genomic stability, the imprinting process, chromatin architecture, and gene expression during placental development in mice. Thus, null mutations in essential genes encoding chromatin-modifying enzymes cause various defects in trophoblast development. Kmt5a−/−, Kat5−/−, and Kat8−/− mutations result in cell death. Kdm1a−/−, Nsd1−/−, Prmt1−/−, Prmt5−/−, Ezh2−/−, and Rnf2−/− mutations result in chorion defects. Ehmt2−/− and Dnmt1−/− result in defects in chorioallantoic fusion. Setd2−/− results in defects in vascular branching. me, methylation; ac, acetylation; p, phosphorylation; ub, ubiquitination; dace, deacetylation; dme, demethylation.

073

Cells & Development @cellsdev.bsky.social · 13/02/2026

Cells moving through tissue interact with the ECM and also with other cells, which can affect morphogenesis. In this interesting paper from the M Lisa Manning lab, Kupffer's Vesicle's trailing cells are shaped by the dragging force from other cells as it moves through tissue. doi.org/10.1016/j.cd...

0123

Cells & Development @cellsdev.bsky.social · 06/02/2026

✂️ the head of round-head worm => new round head formed. ✂️ the head of flat-head worm => new flat head formed. What shape will it be if we ✂️ the head of a worm with 50:50 round + flat stem cells? Check out this exciting review by @drmichaellevin.bsky.social lab! #chimerism doi.org/10.1016/j.cd...

Fig. 1. What determines the anatomical setpoint of regenerative homeostasis?
Planarian flatworms regenerate after amputation using a resident population of stem cells. This process reliably stops when the correct species-specific head shape is restored. The following thought experiment illustrates the profound knowledge gap in our understanding of the rules of morphogenesis despite ample information about genes required for neoblast differentiation. (A) Fragments from a round-head species result in a round-headed regenerate; (B) Fragments from a flat-head species result in flat-headed regenerates. (C) A chimera can be produced by irradiating one species (removing half of the stem cells) and receiving injections of donor neoblasts from a flat-head species. (D) When neoblasts from diverse species combine in the same body, and the head is amputated, what head shape will the regenerative process construct? Despite genomic and molecular-biological information on regeneration in multiple species, the field as yet has no models which make a prediction. This illustrates the importance of chimeras in identifying gaps in our understanding of the rules of emergent processes such as anatomical homeostasis and collective decision-making by cell groups.

094

Cells & Development @cellsdev.bsky.social · 31/01/2026

A fascinating review on the role of Activin in organ induction. Isn't it wild that in Xenopus embryos, a piece of the animal cap can be induced with Activin at different concentrations and buffers to form the ❤️, kidney, the pancreas, head, tail, and even a whole embryoid 🤯: doi.org/10.1016/j.cd...

Fig. 1. Animal cap assay and sandwich method as in vitro induction systems.
In amphibians, a blastocoel cavity clearly forms inside the animal hemisphere during the blastula and early gastrula stages. The cap-like portion lining the roof of the blastocoel cavity is the animal cap. This region consists of a sheet of pluripotent cells, organized into one or several layers. In the animal cap assay, the animal cap was treated with a physiological saline solution containing inducing factors and then cultured. Depending on the type, concentration, and duration of exposure to the inducing factors, animal caps can differentiate into various cell types. In contrast, the sandwich method, involves culturing the inducer source in between two animal caps. In this technique, the sources of induction can include the dorsal lip of the blastopore (organizer), adult tissues, pelletized soluble factors, or animal caps pretreated with soluble factors. In this figure, activin is used as an example of an inducing factor.

Fig. 12. Summary of the in vitro induction system using activin as an inducing factor.
This in vitro induction system utilizes activin and retinoic acid as inducing factors to treat animal caps, employing techniques such as animal cap assay, dissociation/reaggregation protocol, and the sandwich method. By applying these methods, various levels of self-organization can be replicated and controlled in vitro, ranging from lower-order cell differentiation to higher-order tissue differentiation, organogenesis, and even the formation of fundamental body plans. Abbreviations: Dorsal [D], ventral [V], and retinoic acid [RA].

Fig. 11. Formation of embryoids by artificial activin concentration gradients.
To create embryoids, animal caps were prepared through treatment with low (0.5–1 ng/ml), intermediate (5–10 ng/ml), or high (50–100 ng/ml) concentrations of activin. These three types of activin-treated animal caps were then sequentially arranged and cultured with untreated animal caps. After 3 days of culture, embryoids with distinct head and trunk-tail structures were formed (A). Histological sections revealed differentiation into head tissues, such as the cement gland [cg] and eyes, and trunk-tail tissues including the ear vesicle [ev], brain [br], notochord [not], muscle [mus], and gut (B). When newt embryos are used in similar combination cultures, neural plate structures forming the brain [white arrow] and axial structures forming the trunk-tail regions [black arrow] are sometimes observed (C).

Fig. 7. In vitro heart formation and in vivo transplantation experiment.
When treated with a high concentration of activin, the animal caps of Xenopus embryos did not differentiate into heart tissue. However, if the animal cap dissociates into individual cells before activin treatment and then reaggregates, it forms a beating heart [arrow] with 100 % efficiency (A). This heart expresses differentiation marker genes, such as Nkx2.5, GATA-4, Tbx5, MHCα, TnIc (cardiac troponin I), and ANF, none of which are expressed in an animal cap treated with activin alone, without dissociation/reaggregation (B). Electron microscopy reveals the presence of intercalated discs [id] specific to the cardiac muscle, along with visible mitochondria [m] and Z-bands [z] (C). When the reaggregated heart tissue is orthotopically transplanted into the cardiac primordium of a neurula-stage embryo, it integrates without rejection and continues to beat (D), although it does not persist through host metamorphosis. In contrast, when the reaggregated tissue is ectopically transplanted into the ventral region of the neurula, it begins to beat synchronously with the host heart and gradually reddens as it initiates blood circulation (E).

02911

Cells & Development @cellsdev.bsky.social · 23/01/2026

Did you know that melanocytes, chondrocytes, and even osteoblasts can be differentiated from Schwann Cell Precursors? These cells don't only give rise to Schwann cells as the name suggests but many other cell types. Check out this interesting review by Marianne Bronner et al: doi.org/10.1016/j.cd...

Fig. 1. Embryonic origins of Schwann cell precursors. Transverse cross-section through the neural tube showing three pathways giving rise to Schwann cell precursors (orange) that have been discussed in the literature: 1. Neural crest cells (blue) migrate from the dorsal neural tube and give rise to Schwann cell precursors along the dorsal root along which they migrate into the periphery. 2. Neural crest cells (blue) migrate to the site of the future dorsal root entry zone (DREZ) or future motor exit point (MEP) where they give rise to boundary cap cells (green). These boundary cap cells then give rise to Schwann cell precursors along the dorsal and ventral roots. 3. The neuroepithelium (purple) is a currently contested source of Schwann cell precursors along the ventral and possibly dorsal roots. Arrows show direction of migration. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Fig. 2. Schwann cell precursor derivatives. Schwann cell precursors (orange) have been shown to give rise to a diverse range of cell types (blue). Grey circles represent axons, viewed in transverse cross-section. Arrows show direction of differentiation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

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Cells & Development @cellsdev.bsky.social · 17/01/2026

A very curious paper from the De Robertis lab shows how Cerberus - a growth factor that inhibits Wnt signalling, and IGF - a growth factor that activates MAPK signalling, can synergistically induce a new head (aka ectopic archencephalic differentiation) in Xenopus embryos. doi.org/10.1016/j.cd...

Fig. 1. IGF2 and Cerberus mRNAs cooperate in ectopic head induction in Xenopus embryos.

Embryos were microinjected into the ventral marginal zone of a single blastomere at the 4- to 8-cell stage. (A) Uninjected control sibling at early tailbud stage (n = 81). (B) A single ventral injection of IGF2 mRNA caused a small ectopic head protrusion with a pigmented cement gland on the belly (n = 86, 68 % with ectopic structures). (C) Cerberus mRNA induced a secondary head-like structure (n = 78, 94 % with ectopic heads). (D) Co-injection of IGF2 and Cerberus mRNAs induced a large ectopic head with an expanded cement gland (n = 90, 98 % with ectopic heads). (E–H) Panoramic views of control and injected embryos. Injected mRNA doses per embryo were: Cerberus, 100 pg; IGF2, 2 ng. Results from two experiments. Scale bars are 500 μm (A-D) and 2 mm (E-H).

Fig. 6. Dominant-negative IGF receptor 1 blocked ectopic head formation by Cerberus mRNA in single ventral injections.

(A) Control embryo at stage 24 injected with LacZ (100 pg) mRNA but not stained for β-galactosidase (n = 50). (B) DN-IGFR (600 pg) and LacZ injected embryos (n = 20, all normal). (C) Cerberus (100 pg) injected embryos with ectopic heads (n = 56, 96 % ectopic heads). (D) DN-IGFR blocked Cerberus ectopic heads (n = 33, 88 % with no ectopic structures, 12 % with small cement glands). (E–F) LacZ staining for (A–D). Scale bar, 500 μm.

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Cells & Development @cellsdev.bsky.social · 10/01/2026

Organoid technology is one of the most significant advancements deriving from developmental biology. Yet, many aspects of the biology of organoid itself remain elusive, one of which is the role of mesenchymal stem cells. This review: doi.org/10.1016/j.cd... by Wang et al discusses this in detail.

Fig. 1. Timeline of organoids development. The history of organoids was initiated by Ross Harrison's origin of nerve fiber experiments and continues to evolve to the present day.

Fig. 2. Timeline of MSCs development. In 1970, Friedenstein first divided “fibroblast colonies” from guinea-pig bone marrow and spleen. In 1976, “clonogenic fibroblast precursor cells” were discovered in mouse bone marrow. In 1995, the first-in-human trial of MSCs was conducted. In 1999, it was first discovered that MSCs can differentiate in vitro into osteoblasts, adipocytes, and chondrocytes. During the period from 2000 to 2010, key functions of MSCs, including homing and migration, were discovered. In 2018, MSCs entered clinical trials for heart failure and Crohn's disease. From 2021 to 2025, clinical trials for MSCs expanded to include cirrhosis, osteoarthritis, and diabetic foot.

Fig. 3. Schematic illustration of MSC-mediated optimization of organoids: from challenges to future perspectives. Current organoid systems face limitations such as lack of vasculature, central necrosis, and absence of functional immune components. MSCs address these challenges through two main strategies: acting as structural components in co-culture systems (direct relations) and serving as microenvironmental regulators via paracrine signaling and EVs (indirect relations). The integration of MSCs leads to improved organoid outcomes, including promoted angiogenesis, enhanced maturation, and immunomodulation. Future directions involve combining MSC-organoid systems with 3D bioprinting and organ-on-a-chip technologies to facilitate disease modeling, drug screening, and clinical translation.

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Cells & Development @cellsdev.bsky.social · 17/12/2025

Check out the summary written by our Editor in Chief, Professor Roberto Mayor: www.sciencedirect.com/science/arti... And if you missed it, here is the link to Part I of the collection: www.sciencedirect.com/special-issu...

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Cells & Development @cellsdev.bsky.social · 17/12/2025

We're in love with this cover image! 🧡 Part II of our Special Collection celebrating the Centennial of the Discovery of The Organiser is here. This issue focuses on the work presented at the Centennial Symposium at the University of Freiburg in September 2024: www.sciencedirect.com/journal/cell...

Many small photos taken from the symposium organised to reveal Spemann and Mangold in the background.

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Cells & Development @cellsdev.bsky.social · 12/12/2025

Vertebrates can use entirely different mechanisms to generate its anterior and posterior dorsal tissue. In this thorough review from the lab of Lance Davidson, different morphogenetic events are compared between the front and the back in a developing embryo. Check it out: doi.org/10.1016/j.cd...

Fig. 1. Comparative stages of transition from primary-to-posterior dorsal axial tissue formation. A dorsal and sagittal comparison of simplified CNS morphology in at the stage(s) of PNP closure (presumed junctional neurulation) between model organisms commonly used to study neurulation processes. A dorsal view of the shared structural characteristics between vertebrates at the posterior end depicts the anterior portion of the posterior processes which have completed neural tube closure and are in the process of segmenting somites from pre-formed PSM. Dashes mark the regions where primary and secondary neurulation processes occur at the same time and are overlapping (transition zone). Posterior to established neural tube and PSM is the region containing the NMP cell population, which are proliferating and maturing to form PSM and neural tube structures in an anterior to posterior direction. Mammals have formed roughly between 28 and 30 somites at neuropore closure (E9.5–10 in mouse, day 27 in humans). Avian have formed 22 somites at HH13, whereas amphibians have formed only 6–7 somites by NF 20. Finally, zebrafish have 21 somites at 19.5 hpf, which corresponds to the stage of neural primordium elongation, without convergence.

Fig. 2. Antero-posterior progression of neurulation and somitogenesis. A graphical representation of primary and posterior processes that generate identical, uninterrupted structures through a transition zone. All vertebrates begin primary processes with a predetermined superficial neural cell layer, that converges at the midline to form a single lumen and pre-somitic mesoderm that condenses and segregates into somites. Posterior processes are established from a multi-potent NMP cell population that diverge to form separate neural and mesodermal populations and eventually forms structures indistinguishable from primary structures. These processes are hypothesized to occur at the same time within the transition zone, where primary processes progressively transition into posterior processes.

Fig. 3. A comparison of naïve/pluripotent/stem cell populations and organizer regions. An organizer is capable of modulating the cell identities of neighboring cell populations through expression of various BMP antagonists and additional growth factors. Naïve cells are undifferentiated cells that are capable of developing into various cell types, dependent on the externally applied conditions. The diagrams are representative of the transplantation experiments completed by Spemann and Mangold, which illustrates the organizer's ability to induce neural identity from host cells.

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Cells & Development @cellsdev.bsky.social · 06/12/2025

Principles in mechanical engineering can be applied to study biomaterials, such as the notochord. In this theoretical study, Curcio et al investigated how the different ways of notochord stacking affects its structural rigidity. A staircase stacking seems to be better! doi.org/10.1016/j.cd...

Fig. 1. Initial geometries and boundary conditions for pressurization and three-point bending studies.

Fig. 4. Examples of three-point bending. Lateral and/or transverse displacements are nondimensionalized, dividing by initial cell dimension d(init).

Fig. 2. Inflation study: geometric changes.

Fig. 3. Pressure study: resulting tensions.

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Cells & Development @cellsdev.bsky.social · 28/11/2025

Tissue-resident macrophages are doing more than just protecting from infection. In this interesting paper, René Fernando Abarca-Buis et al shows that they can promote reepithelialization and blastema formation and regulate the maturation of chondrocytes. Check it out here: doi.org/10.1016/j.cd...

Fig. 1. Doble immunodetection of CD68 and F4/80 during ear hole regeneration in early postnatal mice.

Fig. 6. Clodronate liposomes treated ears in re-differentiation show acceleration of cartilage maturation.

Fig. 4. Modifications in the regenerative response by the treatment with clodronate liposomes during wound healing phase of early postnatal mice ear hole regeneration.

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Cells & Development @cellsdev.bsky.social · 21/11/2025

It is not often that Sialoglycoproteins and sialyltransferases are mentioned during early development. This interesting review from the lab of Katia Cailliau brings the interesting biology of sialic acid into the context of #devbio, particularly during blastula formation. doi.org/10.1016/j.cd...

Enzymes involved in the biosynthesis pathway of sialic acid, sialic motifs, and sialylated proteins present during cleavage stages in the blastula and blastocyst formation, in embryonic stem cells (ESCs), and during the epithelial-to-mesenchymal transition (EMT) across various species. The production of sialylated proteins follows a multistep pathway derived from the glucose metabolism and occurs across three cellular compartments, ultimately leading to the placement of sialylated proteins in the plasma membrane.

Blastula from various species. The coeloblastula surrounds an inner fluid-filled blastocoel, whereas the stereoblastula shows no cavity. I

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Cells & Development @cellsdev.bsky.social · 07/11/2025

"His secret weapons were an unquenchable curiosity and continuing hands-on experimentation at the bench with his beautiful frog embryos and oocytes". A thoughtful tribute to the life of Sir John Gurdon by Edward M. De Robertis that we really recommend everyone to read. doi.org/10.1016/j.cd...

Sir John Gurdon on the occasion of his 80th birthday.

Original portrait by Prof. Nadia Rosenthal of The Jackson Laboratories, pencil on Arches paper. Courtesy of the artist.

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Cells & Development @cellsdev.bsky.social · 30/10/2025

From the lab of Chinmoy Patra discussing the importance of ECM in heart morphogenesis and the roles of secreted molecules in mediating fibrosis or regeneration after myocardial injury. doi.org/10.1016/j.cd...

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Cells & Development @cellsdev.bsky.social · 30/10/2025

From the lab of Maxwell Heiman discussing the interesting topic of apical ECM and the function of sensing organs and how these ECM proteins can both mechanically and biochemically modulate the organ's functions. doi.org/10.1016/j.cd...

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Cells & Development @cellsdev.bsky.social · 30/10/2025

From the lab of Jean Schwarzbauer identified IGFBP3 as the most up-regulated gene in fibrotic human lung fibroblasts and can be used as a potential biomarker for idiopathic pulmonary fibrosis. doi.org/10.1016/j.cd...

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Cells & Development @cellsdev.bsky.social · 30/10/2025

From the lab of Eva Matalova exploring the role of TGF-B in gld osteoblastic cells. doi.org/10.1016/j.cd...

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