Sachin Kotak

Sachin Kotak

@spindlebehavior.bsky.social

Cell Biologist interested in fundamental cell division processes working @iiscbangalore

92 followers118 following17 posts

Happy to see our work on how Aurora A kinase orchestrates nuclear organization by regulating the material properties of spindle pole–localized NuMA at mitotic exit featured on the cover. Grateful to the students for creating this beautiful image!

The EMBO Journal@embojournal.org

In ISSUE 23 Highligh: IL-26 - no guts, no glory Review: initiating autophagy by selective receptors Method: 3D-SPARK for spatial mapping of DNA synthesis Resource: senotypes across aging human and mouse tissues Cover: Sachin Kotak et al @spindlebehavior.bsky.social link.springer.com/journal/4431...

Happy to share our work in @embojournal 👉 shorturl.at/zXNyn For decades, we’ve known cells dismantle & rebuild the nuclear envelope in sync with spindle poles. But why does this coordination matter? And how do pole material properties ensure error-free division? Follow this thread to know more 👇

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Finally, by tracking nucleolar organization and chromatin–chromatin contacts (via 4C analysis), we show that perturbing nuclear organization directly disrupts chromatin organization at mitotic exit. This work highlights the biological significance of spindle pole disassembly at mitotic exit.

Happy to share our work in @embojournal 👉 shorturl.at/zXNyn For decades, we’ve known cells dismantle & rebuild the nuclear envelope in sync with spindle poles. But why does this coordination matter? And how do pole material properties ensure error-free division? Follow this thread to know more 👇

View full thread

Notably, forcing multimerization of NuMA molecules is sufficient to recapitulate the phenotype seen upon Aurora A inactivation. This indicates that multimerization is the key process disrupted when Aurora A activity is lost.

By restricting Aurora A activity to only one spindle pole, we found that the opposite pole lacking Aurora A activity accumulates “solid” NuMA, which in turn forces the segregated chromosomes to bend around this abnormal pole.

Happy to share our work in @embojournal 👉 shorturl.at/zXNyn For decades, we’ve known cells dismantle & rebuild the nuclear envelope in sync with spindle poles. But why does this coordination matter? And how do pole material properties ensure error-free division? Follow this thread to know more 👇

View full thread

NuMA accumulation at spindle poles depends on: • dynein/dynactin (trucks) • its coiled-coil domain (cranes), and • its ability to form multivalent cation-π interactions through its intrinsically disordered region (IDR) at the C-terminus (hooks in cyan).

Happy to share our work in @embojournal 👉 shorturl.at/zXNyn For decades, we’ve known cells dismantle & rebuild the nuclear envelope in sync with spindle poles. But why does this coordination matter? And how do pole material properties ensure error-free division? Follow this thread to know more 👇

- We found that Aurora A activity in anaphase is crucial for shaping the nucleus during mitotic exit. To probe this, we built a cyclin-B1-based degron tool that enables rapid, phase-specific degradation of Aurora A, right as cells exit mitosis.

When Aurora A is inactivated, we found that NuMA, a conserved spindle pole protein, undergoes a material state transition from dynamic to solid, and abnormally accumulates at the spindle poles. This abnormal “accumulation” causes NuMA segregated chromosomes/nuclei to bend around them.

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