How the autophagy-related E3 complex localizes to pre-autophagosomal structures and a non-E3 function of the complex were revealed, significantly advancing our understanding of the nucleation step in autophagosome formation.
Proteasomes are protected from autophagic elimination upon carbon starvation by sequestration into cytoplasmic storage granules, which aid cell fitness by providing a cache of proteasomes that can be rapidly remobilized when carbon availability improves.
Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.
Two newly identified assembly factors for the ribosome-associated iron-sulfur protein Rli1 reveal a general mechanism for how the cytosolic iron-sulfur protein assembly (CIA) machinery recruits apoproteins.
TORC2-Ypk1 signaling upregulates flux through the sphingolipid pathway not only by increasing the supply of long-chain base precursors, but also by increasing their use in synthesizing complex sphingolipids.
IL-27 exerts differential activation of STAT1 and STAT3 via IL-27Ra and GP130, respectively, leading to a kinetic decoupling of its gene expression program, which contributes to tune its immuno-modulatory activities.