Abstracts due in 2 weeks for the Signal Dynamics FASEB! Many speaking slots will be filled from submitted abstracts

events.faseb.org/event/Dynami...

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

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

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.

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

Developmentally inspired synthetic kidney engineering Nature Biotechnology - Hughes and colleagues present a developmentally inspired tissue engineering strategy to overcome barriers in kidney tissue generation, enhancing prospects for renal...

Check out our new @natbiotech.nature.com review on how to build kidneys & other epithelial organs using principles from embryonic development. Led by Emma Warrner and @azyhuang.bsky.social.

www.nature.com/articles/s41...

rdcu.be/e3fy0

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

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.

Now in print at ACS Synbio! Introducing Aviatar: a concept for inducible translocation to any cell compartment using only a 1-component probe
pubs.acs.org/doi/10.1021/...

Our new paper just out!
pubs.acs.org/doi/10.1021/...

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.

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

lol real love

Self-folding laundry YouTube video by PrakashLab

(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...

EGFR suppression and drug-induced potentiation are widespread features of oncogenic RTK fusions Regulation of cancer cells by their environment contributes to tumorigenesis and drug response, though the extent to which the oncogenic state can alter a cell’s perception of its environment is not c...

See also a concurrent preprint showing that diverse RTK fusions can suppress transmembrane EGFR. These other fusions also mostly did *not* form condensates, but did form small, active multimers.

www.biorxiv.org/content/10.1...

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!

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.

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

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.

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.

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.

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.

🚨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...

👇

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

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.

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).

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

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

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...

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