Embryonic PI3K-Yap activity regulates apical adhesion and proliferation of neural progenitors lining the lateral ventricular surface, to maintain the smooth, non-folded mouse brain and to prevent developmental hydrocephalus.

CFAP52 is a candidate for genetic diagnosing male infertility with defects of sperm head-tail connection and flagella development.

Acute one-hour treatment of Pik3ca mutant mice with a novel anti-epilepsy drug suppresses seizures despite continued developmental brain dysmorphology, promising a new therapeutic strategy for patients with intractable pediatric epilepsy.

Mice doubly deficient for Naa10 and Naa12 display embryonic lethality, with both enzymes compensating for each other with amino-terminal acetylation of proteins in mouse development.

A mouse model where the splicing factor SRSF1 was prevented from accumulating in the cytoplasm revealed reduced translation of thousands of mRNAs and postnatal phenotypes particularly affecting multiciliated cells.

Mirroring human patients with ARID1B mutations, Arid1b haploinsufficient mice exhibited numerous neuropsychiatric defects and revealed IGF1 deficiency related growth impairment that could be ameliorated with growth hormone supplementation.

Centriolar satellites facilitate efficient trafficking of proteins to and from centrioles and are required for early steps of cilia formation and timely ciliogenesis in vivo, where mice lacking satellites display perinatal lethality, hydrocephalus, oligospermia, and cerebellar hypoplasia.

Cryo EM and a custom subvolume refinement approach applied to mouse polyomavirus revealed the in vivo impact of polyomavirus capsid mutations on antiviral antibody immunoevasion and neurovirulence.

Non-specific sodium entry inhibits T cell receptor induced gene expression and differentiation of T cells by depleting intracellular ATP and disrupting mTORC2 dependent signalling axis.

Unbiased transcriptome analyses reveal that neural progenitor cells downregulate protein biosynthetic machinery during early forebrain development, and this fundamental process matches proteomic changes in the adjacent cerebrospinal fluid and is regulated in part by MYC.