Drosophila Golgi membrane protein Ema promotes autophagosomal growth and function

2. Zero hunger 0301 basic medicine Monosaccharide Transport Proteins Fat Body Golgi Apparatus Genes, Insect Endosomes Membrane Fusion 03 medical and health sciences Microscopy, Electron, Transmission Phagosomes Mutation Autophagy Animals Drosophila Proteins Humans Drosophila Lectins, C-Type Lysosomes
DOI: 10.1073/pnas.1120320109 Publication Date: 2012-04-10T01:05:20Z
ABSTRACT
Autophagy is a self-degradative process in which cellular material enclosed within autophagosomes and trafficked to lysosomes for degradation. Autophagosomal biogenesis well described; however mechanisms controlling the growth ultimate size of are unclear. Here we demonstrate that Drosophila membrane protein Ema required autophagosomes. In an ema mutant, form response starvation developmental cues, these can mature into autolysosomes; very small, autophagy impaired. fat body cells, localizes Golgi complex recruited starvation. The Lva also periphery starvation, this recruitment requires . Therefore, propose source autophagosomal facilitates process. Clec16A, human ortholog Ema, candidate autoimmune susceptibility locus. Expression Clec16A rescue autophagosome defect suggesting regulation morphogenesis may be fundamental function gene family.
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