In Drosophila oocytes, the exclusion of the scaffold protein PAR3 from the posterior cortex depends on PAR1 and endocytosis, while its anterior localisation requires microtubules and recycling endosomes.
TRPV4 channels in brain capillaries are suppressed by the phosphoinositide PIP2 and activated by receptor agonists implicated in neurovascular coupling.
Epidermal cells in vertebrates and invertebrates ensheath portions of somatosensory neurons via a conserved morphogenetic mechanism, and this ensheathment regulates morphogenesis and function of Drosophila nociceptive neurons.
Synergistic interactions with PI(4,5)P2 and activated Rho1, which are enriched at the apical membrane of tubular organs, facilitate tight apical targeting of the formin Diaphanous.
Genetic and biochemical analysis of two enzymes reveals that inositol pyrophosphate signaling molecules allow plants to sense and regulate cellular phosphate levels, and to take up more phosphate when needed.
A Notch-mediated signaling pathway upregulates a Sec14-GOLD phosphopholipid binding protein that promotes a morphogenetic process important in tissue remodeling and renewal.
Studies of Lowe syndrome patient cells, which lack the inositol 5-phosphatase OCRL, suggest that a defect in endocytosis plays a role in the pathological manifestations of the disease.
