To control centriole duplication, centriolar satellite proteins assemble a microcephaly-associated protein complex at the centrosome and activate cyclin-dependent kinase 2.

Structural analyses of the centriole proteins CPAP and STIL identify domains that are critical for centriole formation and provide a structural explanation for a mutation that causes human microcephaly.

Microcephaly-associated mutations disrupt microtubule-dependent WDR62 translocation from the Golgi complex to the mitotic spindle poles, impair mitotic progression, and alter neurogenic trajectories in patient induced Pluripotent Stem Cell-derived 2D and 3D models of human neurodevelopment.

The previously uncharacterized protein PPP1R35 is a novel centriolar luminal protein critical for centriole elongation by acting in a complex with microcephaly protein RTTN.

An ento-epidemiological model reveals that what made the Zika virus a public health problem in Feira de Santana, Brazil, was a surprisingly high attack rate coupled with a low risk of Microcephaly per challenged pregnancy.

Non-centrosomal microtubule nucleation mediated by augmin is essential for neural progenitor mitosis and survival, and thus brain development.

The structural maintenance of chromosomes complex, SMC5/6, is crucial for brain development and function as it ensures proficient DNA replication in neural progenitor cells prior to chromosome segregation.

That early cortical neural progenitor divisions strictly require OCLN isoform expression is a paradigm shift in the functional consideration of this protein best known for promoting between-cell barrier functions.

Chromosome condensation by condensin II is inhibited during interphase by direct interaction with MCPH1, which regulates opening of the condensin II interface between SMC2 and NCAPH2, in a similar fashion to how WAPL regulates Cohesin.