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
AUTHORS (3)
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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