Publications by authors named "Lenaig Defachelles"
Spindle checkpoint strength is dictated by the number of unattached kinetochores, cell volume, and cell fate. We show that the conserved AAA-ATPase PCH-2/TRIP13, which remodels the checkpoint effector Mad2 from an active conformation to an inactive one, controls checkpoint strength in . Having previously established that this function is required for spindle checkpoint activation, we demonstrate that in cells genetically manipulated to decrease in cell volume, PCH-2 is no longer required for the spindle checkpoint or recruitment of Mad2 at unattached kinetochores.
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- The activity of Mad1 at kinetochores is crucial for the spindle assembly checkpoint (SAC), which prevents anaphase from starting if kinetochores aren't properly attached to spindle fibers.
- The RZZ complex (Rod, Zw10, Zwilch) is key for recruiting Mad1 to kinetochores, but how this happens isn't fully understood.
- This study shows that while Mad1 has a dynamic presence at unattached kinetochores with a half-life of 12 seconds, RZZ remains stable, and there's a physical association between Mad1 and RZZ.
Proper kinetochore recruitment and regulation of dynein and the Mad1-Mad2 complex requires the Rod-Zw10-Zwilch (RZZ) complex. Here, we describe rod(Z3), a maternal-effect Drosophila mutation changing a single residue in the Rough Deal (Rod) subunit of RZZ. Although the RZZ complex containing this altered subunit (denoted R(Z3)ZZ) is present in early syncytial stage embryos laid by homozygous rod(Z3) mothers, it is not recruited to kinetochores.
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