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.
Genetic and molecular analyses identify and characterize an evolutionary battle over lysis timing wherein a bacteriophage delays lysis through lysis inhibition while a defensive phage satellite accelerates lysis.
TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
Phosphorylation-mediated inactivation of pro-apoptotic BCL-2 family protein BAD confers the apoptosis resistance on synovial sublining macrophages, thereby contributing to the development of rheumatoid arthritis.
Extensive cytological and biochemical analyses show that the conserved Sf3A2 and Prp31 splicing factors bind microtubules and the Ndc80 complex, playing direct mitotic functions in both Drosophila and human mitosis.