An in-depth metagenomic analysis of possibly the most abundant and widespread microbial lineage in the surface ocean teases apart evolutionary processes that maintain its genomic heterogeneity and biogeography.
Cryo-EM shows that the NADase activity of SARM1 is allosterically inhibited by physiological concentrations of NAD+ that stabilizes an auto-inhibited conformation of SARM1, explaining how NAD+ depletion may inflict neurodegeneration.
Axonal metabolic flux analysis demonstrates that expression of NMNAT1 blocks axonal degeneration in cultured mouse neurons not by altering NAD+ synthesis, but rather by inhibiting injury-induced, SARM1-dependent NAD+ consumption.
A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.
Genetic and biochemical analyses reveal a virulence mechanism employed by V. dahliae that involves inhibition of the transcription factor activity of CBP60g and SARD1.
A structure of the complete, membrane bound, COPII coat solved by sub-tomogram averaging reveals the arrangement of all protein subunits on the membrane and suggests a mechanism for coating heterogeneously-shaped carriers.
Ppg1-dependent assembly of the mitochondrial Far complex and association/dissociation between the Far complex and Atg32 are crucial determinants for mitophagy regulation in yeast.
Building on previous work (Nogueira et al., 2014), we describe a mechanism for the generation of a mega-carrier for the export of bulky procollagen from the endoplasmic reticulum.
Building on previous work (Ge et al., 2013), it is shown that the ER-Golgi intermediate compartment is a platform for the production of COPII vesicles as precursor membranes for the lipidation of LC3, which is an essential step in autophagosome biogenesis.
