MIT's Robert Horvitz and his colleagues show in a Cell paper published online in advance this week that "the CAF-1 protein complex, an evolutionarily conserved histone chaperone that deposits histone H3-H4 proteins onto replicating DNA, is required to generate a bilateral asymmetry in the C. elegans nervous system." Horvitz et al. also show that a mutation in one of 24 histone H3 genes in the roundworm eliminates this asymmetry, due to the inhibition of CAF-1-mediated nucleosome formation caused by a defect in the formation of a histone H3-H4 tetramer.
Over in Cell Reports, a team led by investigators at the University of California, San Francisco, reports on four truncating mutations involving PRRT2 that they identified in paroxysmal kinesigenic dyskinesia with infantile convulsions, or PKD/IC, patients. The team first identified these PRRT2 mutations in 24 of 25 well-characterized PKD/IC-affected families, and later in 28 or 78 additional families.
Yale University School of Medicine's Michael Caplan and his colleagues report in Developmental Cell that the "loss of polycytin-1 expression results in increased proliferation and apoptosis" such that the γ-secretase-dependent release of its carboxy-terminal tail "creates a protein fragment whose expression is sufficient to suppress ADPKD [autosomal-dominant polycystic kidney disease ]-related phenotypes in vitro and in vivo."