p53 deletion rescues lethal microcephaly in a mouse model with neural stem cell abscission defects.

Building a cerebral cortex of the proper size involves balancing rates and timing of neural stem cell (NSC) proliferation, neurogenesis and cell death. The cellular mechanisms connecting genetic mutations to brain malformation phenotypes are still poorly understood. Microcephaly may result when NSC divisions are too slow, produce neurons too early or undergo apoptosis but the relative contributions of these cellular mechanisms to various types of microcephaly are not understood.

Mutation of Kinesin-6 Kif20b causes defects in cortical neuron polarization and morphogenesis.

Background: How neurons change their cytoskeleton to adopt their complex polarized morphology is still not understood. Growing evidence suggests that proteins that help build microtubule structures during cell division are also involved in building and remodeling the complex cytoskeletons of neurons. Kif20b (previously called MPP1 or Mphosph1) is the most divergent member of the Kinesin-6 family of "mitotic" kinesins that also includes Kif23/MKLP1 and Kif20a/MKLP2.