Mutations in KIAA0586 (TALPID3) cause a severe ciliopathy called Joubert syndrome that affects organ, cell and centrosome polarity.

DynAPs reveal that biological phase separation provides the organizing principle for the complex process of dynein motor assembly in cells with motile cilia.

Genetic studies in mice reveal the molecular and embryological mechanisms of vocal fold development and function, thereby informing our understanding of vocal communication and congenital voice defects.

Cells have evolved a mechanism that actively regulates centriole maturation during quiescence.

A supervised learning approach on a high-content genome-wide siRNA screen has identified 591 likely candidates for ciliopathies and facilitated in the discovery of KIAA0586 mutations in individuals with Joubert syndrome.

Chaperoning defects in axonemal dynein subunits trigger proteostatic clearance of dynein motors opening up the possibility of trialling proteostasis modulators to treat the motile ciliopathy primary ciliary dyskinesia (PCD).

The proper development of the vocal cords requires embryos to contain a certain number of progenitor cells, and mutations that lead to an overflow of cells can cause malformations of the voice box.

A small GTPase within the flagellum can participate in the control of transport from the base to the tip of the flagellum, and back again.

The anaphase promoting complex (APC) has an essential role in ubiquitin-mediated proteolysis in the disassembly of cilia.

The ciliary G-protein Arl13B – which is often mutated in Joubert syndrome – is the Guanine nucleotide exchange factor for the G-protein Arl3 and exclusively localizes to cilia.