AI Article Synopsis
- Polarized cells depend on a specialized cytoskeleton, but it's unclear how polarity cues influence this polarization.
- Researchers used advanced 2D protein arrays to manipulate cortical polarity during cell division, helping to understand how polarity signaling leads to cytoskeleton changes.
- Their findings reveal that clustering of Par complex proteins is enough to trigger their assembly, and that this process plays a key role in establishing asymmetric features in cell division, such as spindle orientation and central spindle asymmetry.
Article Abstract
Polarized cells rely on a polarized cytoskeleton to function. Yet, how cortical polarity cues induce cytoskeleton polarization remains elusive. Here, we capitalized on recently established designed 2D protein arrays to ectopically engineer cortical polarity of virtually any protein of interest during mitosis in various cell types. This enables direct manipulation of polarity signaling and the identification of the cortical cues sufficient for cytoskeleton polarization. Using this assay, we dissected the logic of the Par complex pathway, a key regulator of cytoskeleton polarity during asymmetric cell division. We show that cortical clustering of any Par complex subunit is sufficient to trigger complex assembly and that the primary kinetic barrier to complex assembly is the relief of Par6 autoinhibition. Further, we found that inducing cortical Par complex polarity induces two hallmarks of asymmetric cell division in unpolarized mammalian cells: spindle orientation, occurring via Par3, and central spindle asymmetry, depending on aPKC activity.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10765089 | PMC |
| http://dx.doi.org/10.1016/j.cell.2023.08.034 | DOI Listing |
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