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Jessica Mella @jmella.bsky.social · 21/09/2026

5/ Our model is that cells monitor lamin filament assembly and target misincorporated subunits for degradation. The extent of this flux varies by cell type, as do the downstream consequences. The mechanism of these differences is still unknown, but now we have some tools to tackle that question!

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Jessica Mella @jmella.bsky.social · 21/09/2026

4/ Our mutational scan identified polymer interfaces that, when mutated, cause profound protein instability. Interestingly, this destabilization was more severe in differentiated cardiac cells, and cardiomyocytes tolerated these mutations poorly.

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Jessica Mella @jmella.bsky.social · 21/09/2026

3/ We built a landing pad platform to introduce ~18,000 cDNA variants into a safe harbor locus of hiPSCs, then differentiated them into cardiomyocytes and epicardial progenitor cells to assay how cardiac cells handle mutated lamin proteins.

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Jessica Mella @jmella.bsky.social · 21/09/2026

2/ Lamin A is a broadly expressed nuclear intermediate filament with hundreds of associated pathogenic mutations, which have puzzlingly severe effects on the heart. Defining what a loss-of-function mutation is for a scaffolding protein is a challenge, especially since we don't have a structure!

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Reposted by Jessica Mella

Kathy Roberts Forde @krforde.bsky.social · 02/08/2025

Columbia. Harvard. UPenn. George Mason. UVA. UCLA. One by one, universities are being attacked—financially, politically, ideologically. Faculty & staff: don’t wait for it to hit your campus. Join the national movement defending higher ed. standtogetherhighered.org (sign up on homepage)

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