iiinova — where your digital self keeps evolving

Lastly, a big thank you to my fabulous wife Ivel and our 2 boys for unending support and keeping me grounded. And for an additional year on the tenure clock;)

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Also big thanks to former advisors David Schaffer and Wendell Lim for continued mentorship and for showing me how to do this job well.

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Penn BE has been a fantastic place to launch a lab, with maximally supportive leadership(Chairs Dave Meaney and Ravi Radhakrishnan, and Dean Kumar, and world-class colleagues who doubled as close mentors, esp. Arjun Raj, Ken Zaret, Lewis Chodosh.

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Zikang (Dennis) Huang @dennishuang.bsky.social · 21/06/2026

A bit late but…Tenured! Immense gratitude for those who got us here. Firstly the students/postdocs (too many to list!) who took a chance on an unproven lab and were unafraid to pursue some strange new ideas. I couldn't have predicted our path, and I couldn’t be more excited for what's next.

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Reposted by Lukasz Bugaj

Wanna know more about a photoreceptor that encodes a signal adaptation circuit in a single protein, its evolution, and how we engineer it into different info processing modes? Check out poster #26 (and flash talk!) on Tuesday at FASEB signaling!

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Lukasz Bugaj @bugajlab.bsky.social · 04/05/2026

Highlights: Keynotes: Tobias Meyer and Jin Zhang Sessions on metabolism, development, stress, immune, cell cycle, optogenetics, image analysis Workshops on advanced microscopy, organoids Meet-the-experts: academia, industry, publishing Networking (+line dancing!) in Nashville Early reg. ends 5/10!

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Lukasz Bugaj @bugajlab.bsky.social · 04/05/2026

Missed the deadline to submit an abstract to #FASEB Dynamics and Encoding in Cell Signaling (June 21-25)? Fear not: abstract deadline has been extended for 1 more week, until *Sunday May 10*. Several speaker slots and travel awards remain! events.faseb.org/event/Dynami... #CellSigSRC

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Lukasz Bugaj @bugajlab.bsky.social · 23/04/2026

Abstracts are due this Sunday, April 26th! ⏰ Come present your latest work to a fantastic community of researchers interested in all aspects of how cell signal dynamics regulate biological function. events.faseb.org/event/Dynami...

events.faseb.org

Abstracts/Presentations - Dynamics and Encoding in Cell Signaling.

Explore advances in cell communication, signaling, and imaging tech at this unique conference, bridging diverse molecular pathways and systems biology.

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Reposted by Lukasz Bugaj

FASEB @faseborg.bsky.social · 09/04/2026

Encode the cell signals for this "dynamic" conference! Featuring keynotes Tobias Meyer of @weillcornell.bsky.social and @jinzhanglab.bsky.social, alongside organizers Mary Teruel, Eric Batchelor, @bugajlab.bsky.social, and Andrew Paek. Register and submit your abstract by April 26: buff.ly/YMRzst4

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Lukasz Bugaj @bugajlab.bsky.social · 08/04/2026

The Hughes lab @hugheslabpenn.bsky.social develops a robust optogenetic RET receptor and shows it can drive shape changes characteristic of kidney development. Will be exciting to see how opto can help us comprehend development of complex tissue structures

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Lukasz Bugaj @bugajlab.bsky.social · 23/03/2026

Abstract submission now open for the Signaling Dynamics FASEB in Nashville (6/21-25, 2026)! events.faseb.org/event/Dynami... Many speaking slots from submitted abstracts, with a focus on emerging work from trainees and early-career. Come for the science, stay for the line dancing.

events.faseb.org

Abstracts/Presentations - Dynamics and Encoding in Cell Signaling.

Explore advances in cell communication, signaling, and imaging tech at this unique conference, bridging diverse molecular pathways and systems biology.

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Reposted by Lukasz Bugaj

Lukasz Bugaj @bugajlab.bsky.social · 12/01/2026

Speaker lineup posted for FASEB: Dynamics and Encoding in Cell Signaling (June 2026)! Live-cell imaging, biosensors, signal dynamics, and quant. modeling/analysis, across the biosciences. Stellar lineup, Keynotes from Tobias Meyer and Jin Zhang Join us in Nashville! tinyurl.com/bd9wmyve

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Reposted by Lukasz Bugaj

Zikang (Dennis) Huang @dennishuang.bsky.social · 09/02/2026

@GRC photoreceptor and signal transduction now! Please come and check my poster #22 on single proteins that’s adaptive to light stimulation!

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Lukasz Bugaj @bugajlab.bsky.social · 02/02/2026

Thanks Olivier! If you mean recruiting proteins to subcellular compartments--yes. If you mean rearranging organelles within the cell, we thought about it but have not tried it out.

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Reposted by Lukasz Bugaj

Joel Boerckel @jboerckel.bsky.social · 11/01/2026

Defending PhD student, looking over their thesis: “If I knew then what I know now, I could’ve done all of this in like 9 months.” A thread about my favorite pioneering cave explorers and why I don’t think AI will ever “solve” biology.

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Lukasz Bugaj @bugajlab.bsky.social · 12/01/2026

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Reposted by Lukasz Bugaj

Prakash Lab at Stanford @prakashlab.bsky.social · 19/12/2025

(1/n) What if you never had to make your bed? What if your laundry could fold itself? Folding is everywhere around us - but did you know that folding flat sheets are at the ❤️ of diversity of shapes in the animal world - since 500 million years ago. Our latest work: www.youtube.com/watch?v=nudC...

youtube.com

Self-folding laundry

YouTube video by PrakashLab

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Summary: small fusion multimers are sufficient (tho not necessary!) to drive signaling and tumors. While condensates can form, they appear incidental. But if not condensates, then how do fusions signal from the cytoplasm? More to come here!

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5) Finally, a panel of other oncogenic RTK fusions shows that only few form condensates, and none show correlation between condensation and signaling at single-cell.

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4) Unexpectedly, even cytoplasmic *monomers* (const. active) can drive signaling and tumor formation, despite complete lack of multimerization that is essential for condensation.

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3) If condensates are dispensable, diffuse (non-condensing) ALK fusions should be able to signal and drive tumor growth. Indeed they can! Synthetic, cytoplasmic ALK dimers don’t condense but do signal, and also form tumors in mice.

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2) There is lots of active oncogene (pALK) in the diffuse phase, and when treated with ALK inhibitor, timescale of decay in the diffuse phase matches that of downstream signals, but decay in condensates is much slower.

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Evidence of dispensability? 1) EML4-ALK condensation is biphasic (highest at mid levels), but signaling increases monotonically w expression. Thus the strongest signaling is in cells with *no* condensates.

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The condensate (large foci) model suggests that condensates of fusions (e.g. EML4-ALK) are an essential organizer of signaling in the cyto, in the absence of membrane. Causality is unclear though because perturb's of condensates are often also perturb's of kinase activity.

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🚨Preprint 2/2: Several studies implicate condensates in RTK fusion onco-signaling. So we were surprised to find that condensates are entirely dispensable😮(!). A study from proteins to mice, by dynamic duo @davidgonzmar.bsky.social and @trmumford.bsky.social. www.biorxiv.org/content/10.6... 👇

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tagging first author @carolgyz.bsky.social. Congratulations Carol!!

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In sum, RTK fusions are simultaneously activators AND suppressors of mitogenic signaling. We expect future studies can exploit this suppressive behavior for biomimetic therapies designed to enhance killing & combat drug tolerance.

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Finally, synthetic optogenetic RTK fusions demonstrated the key principles: 1) Grb2 binding and sequestration could be decoupled from fusion signaling, and 2) Grb2 sequestration in the cyto is sufficient to desensitize cells to EGFR stim (without signaling).

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Targeted therapy (kinase inhibitors) releases Grb2 and relieves suppression. Potential therapeutic importance because drugs permit receptor signaling that promotes tolerance.

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Mechanism? Fusions sequester adapters like Grb2 in cyto and prevent translocation to active EGFR at membrane. Previously shown for EML4-ALK, below for TPM3-ROS, same for (almost) all fusions tested

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Main surprise: condensates (large foci) are *not* important for EGFR suppression. For EML4-ALK, condensates co-occur with suppression, but for most fusions -- no condensates. See concurrent preprint for more surprises on the role of condensates in fusions. www.biorxiv.org/content/10.6...

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Main finding: Across a panel of 10 oncogenic fusions and patient-derived cell lines, active fusions broadly suppressed the cell’s response to EGF.

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Previously we’d shown that EML4-ALK (onco-fusion) doesn’t only drive cancer signaling—it also suppresses EGFR, and suppression was reversed during therapy. www.nature.com/articles/s41.... Do other fusions also suppress EGFR? Also EML4-ALK formed condensates -- are condensates important?

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