Kinesin-1 alternately moves its two motor domains (heads) to walk along the microtubule. Makino et al. demonstrate that the detached head cannot rebind to the rear binding site because of an intolerable increase in tension, thus ensuring forward stepping after ATP binding.

This work introduces a novel and innovative tagged Col4a1 mouse model for studies of basement membrane dynamics. The authors elucidate important details of COL4A1 turnover in cerebral vasculature and demonstrate that Col4a1 heterozygous deletion is better tolerated than missense mutations.

Death of dopaminergic neurons in the brain is a hallmark of Parkinson’s disease. Gregori and colleagues show that deviant calcium signals in familial disease models caused by mutations in LRRK2 can be reversed by targeting lysosomal TPC2 channels and that TPC2 mimics disease effects in vivo.

Peng Huang et al. find that the ciliary kinesin OSM-3 exhibits an extended, active conformation at the ciliary base and middle segments. Their results indicate the NEK family kinases and PP2A phosphatase collaborate through a phosphorylation-mediated mechanism to regulate the regional motility of ciliary kinesin.

Mammalian cells eliminate nascent chains stalled during co-translational protein translocation by activating a ribosome UFMylation-dependent TAQC process at the ER. Our study establishes a role for NEMF-mediated CAT tailing in TAQC, targeting defective nascent chains for degradation via an unconventional ERAD mechanism.

Nita et al. show that the FGFR2 localizes to primary cilia of the developing mouse tissues and in vitro cells; they identify the molecular mechanism of this action, and show its critical function in FGFR2 signaling.

The authors show that anillin mediates unilateral cytokinesis by blocking the effector binding site of active RhoA. The interaction between active RhoA and anillin is strengthened by anillin’s disordered linker region and is differentially controlled at the slow and fast ingressing sides of the contractile ring.