The crenarchaeon Sulfolobus synthesizes the N-glycan core in the identical way as all Eukaryotes, which strengthens the hypothesis that the eukaryotic N-glycosylation is acquired from an ancient archaeon during eukaryogenesis.

A mechanistic dissection of how autophagy kinase Atg1 is activated in fission yeast reveals surprising differences from the known Atg1 activation mechanisms previously defined in budding yeast.

An image-based multiplex autophagosome RNAi screen targeting all Rab GTPases as well as their GAPs and GEFs identifies the Rab GEF SMCR8 as multifaceted autophagy modulator, which regulates kinase activity and gene expression of ULK1.

The dynamic phosphorylation of autophagy component WIPI2B is critical to maintain autophagosome biogenesis in neurons, and ectopic expression of WIPI2B can restore rates of autophagosome biogenesis in aged neurons.

Hydrogen-deuterium exchange, electron microscopy, and vesicle reconstitution show how binding of the autophagy adaptor NDP52 to the FIP200 subunit of the ULK1 complex triggers membrane binding in autophagy.

A novel mechanism by which a compartment-specific AAA+ complex mediating organelle biogenesis and protein quality control staves off induction of selective autophagy.

Experimental evolution of yeast models of congenital disorders of glycosylation reveals that reduction, but not loss, of phosphoglucomutase activity best compensates for impaired phosphomannomutase activity.

The crosstalk between autophagy and the phagocytosis of apoptotic cells, two cellular clearance pathways, promotes the fusion of the double-membrane autophagosomes to the phagosomes and plays an important role in the degradation of engulfed apoptotic cells.