Volume 14 Issue 7, July 2013

KAT5 Tyr phosphorylation senses chromatin damage and couples this to ATM activation.

A previously undescribed kinesin coordinates the interaction between microtubules and F-actin to ensure a faithful cytokinesis.

Cooperation between α5β1 and αv integrins optimizes the response to fibronectin.

Human embryonic stem cells have been generated through somatic cell nuclear transfer.

ULK1 activates VPS34 by phosphorylating beclin 1 during autophagy induction.

GumbyandOTULINencode a conserved DUB that specifically cleaves linear ubiquitin chains.

The identification of XBP1 as the target of IRE1α in the UPR.

Secreted QSOX1 is required for the incorporation of laminin into the extracellular matrix.

Cofilin severing activity can generate free actin filament ends that are accessible for F-actin polymerization and depolymerization. The combination of structural data for filament severing with recently discovered mechanisms for cofilin activation in migrating cells is increasing our understanding of how cofilin activity affects cell behaviour.

The founding member of the Hedgehog (HH) family of secreted proteins was cloned two decades ago. The mechanism of HH signalling is incomplete, but insight has been gained into the function of lipidation in ligand secretion and transport, as well as into key components of the signalling pathway.

Traditionally, the integrin activity status was thought to be regulated by activators (talin and kindlin), with integrins passively adopting an inactive state. However, it is now emerging that the integrin activity state is dynamically regulated, with inactivators (SHARPIN, ICAP1 and filamin) having a key role in dampening integrin function in different cellular contexts.

The function and regulation of poly(ADP-ribosyl)ation is partially understood. By contrast, little is known about intracellular mono(ADP-ribosyl)ation (MARylation) by ADP-ribosyl transferases. Recent findings indicate that MARylation regulates signalling and transcription by modifying key components in these processes, and that specific macrodomain-containing proteins 'read' and 'erase' this modification.

Early mammalian blastocyst patterning involves symmetry breaking leading to lineage segregation. The classic models of lineage segregation cannot account for recent experimental data, and a new framework that regards the early mammalian embryo as a self-organizing system is put forward to explain these observations.