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Kunal Shroff

@kunalshroff.bsky.social

UCSF MD/PhD in the Kampmann Lab Synapse enthusiast and amateur baker

Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

I am enormously grateful for the countless hours that you all put towards this project to uncover a novel facet of synaptic biology!

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

Thank you to my mentor @kampmann.bsky.social , key collaborators, Lily Jan and @mpownall.bsky.social , my superstar synapse squad within the Kampmann Lab: Molly O’Brien, Tyler Smith, Jialing Fang, and Kelly Yu, and all of my other coauthors!

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

Our findings suggest a mechanism for local integration of synaptic activity information to control glial pruning of those very same synapses!

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

We further discovered that ANO3 colocalizes with ER calcium channel ITPR1 within the postsynaptic compartment to form a postsynaptic signaling platform that drives spatially restricted phosphatidylserine exposure.

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

We applied COMPASS-seq to the in vivo neuronal synapse to uncover a key role for calcium-dependent phosphatidylserine scramblase ANO3 in regulating synaptic numbers during development.

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

However, the precise molecular players that drive exposure of these "eat-me" signals at specific synapses have been unknown. To address this question, we developed a new scalable CRISPR screening approach, COMPASS-seq, to uncover the genetic mechanisms underlying subcellular phenotypes!

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

We know that glial cells play a key role in eliminating neuronal synapses during both development and disease. Glial cells seem to respond to local exposure of "eat-me" signals, such as phosphatidylserine, on the surface of vulnerable synapses.

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Kunal Shroff @kunalshroff.bsky.social · 30/06/2026

I am so excited to share our new preprint! www.biorxiv.org/cgi/content/... This work uncovers a key molecular mechanism that control synapse-specific exposure of the canonical “eat-me” signal phosphatidylserine!

biorxiv.org

Synaptic activity controls local exposure of an 'eat-me' signal via ANO3-ITPR1 signaling

Neuronal synapses are eliminated during brain development and disease through pruning by glial cells. Individual synapses are marked for engulfment by 'eat-me' signals, which include externalized phos...

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