In This Issue
People & Ideas
APC/CCdh1-dependent degradation of USP1 allows for PCNA monoubiquitination and subsequent recruitment of trans-lesion synthesis polymerase to UV repair sites.
Septin GTPases spatially guide microtubule organization and plus end dynamics in polarizing epithelia
Filamentous and microtubule-associated septin GTPases guide the reorganization of the microtubule network during epithelial cell polarization.
Transient cleavage failure in dividing cells is not sufficient to establish stable populations of cells with extra centrosomes.
Nuclear accumulation of AMPK-α1 induces brain atrophy, neuronal loss, and formation of Htt aggregates in a Huntington’s disease model.
The histone chaperone HJURP is a chromatin assembly factor that recruits CENP-A nucleosomes to centromeric chromatin.
Preferential binding of a kinesin-1 motor to GTP-tubulin–rich microtubules underlies polarized vesicle transport
The high affinity of KIF5 for microtubules rich in GTP-tubulin results in polarized motor protein accumulation at axonal tips in neurons and may underlie polarized vesicle transport.
Phosphatidylserine exists lumenally in the ER, Golgi, and mitochondria but cytoplasmically in the trans-Golgi and at the plasma membrane, which suggests that functionally important flipping may occur during trafficking.
nSMase2, which cleaves sphingomyelin to generate bioactive lipids, is required for chondrocyte apoptosis and, cell autonomously, for bone mineralization.
P120RasGAP competes with Rab21 for binding to the cytoplasmic domain of integrin α-subunits, thereby promoting receptor escape from early endosomes and recycling to the plasma membrane.
ICAP-1 prevents recruitment of kindlin-2 to β1 integrin to control dynamics of fibrillar adhesion sites, fibronectin deposition, and osteoblast mineralization during bone formation.
Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons
Neuroligins and leucine-rich repeat transmembrane proteins are necessary to prevent activity-dependent elimination of excitatory synapses in cultured neurons, with synapse elimination operating by a Ca2+/calmodulin-dependent pathway.
A newly identified splice variant of STIM1 called STIM1L forms constitutive clusters that interact with actin and Orai1 and allows fast repetitive Ca2+ release.