Journal
JOURNAL OF CELL BIOLOGY
Volume 173, Issue 6, Pages 963-974Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200511140
Keywords
-
Categories
Funding
- NICHD NIH HHS [T32 HD007480, T32 HD007480] Funding Source: Medline
- NIGMS NIH HHS [R01 GM0625009, R01 GM062509] Funding Source: Medline
Ask authors/readers for more resources
Target of rapamycin (TOR) is a central regulator of cellular and organismal growth in response to nutrient conditions. In a genetic screen for novel TOR interactors in Drosophila melanogaster, we have identified the clathrin-uncoating ATPase Hsc70-4, which is a key regulator of endocytosis. We present genetic evidence that TOR signaling stimulates bulk endocytic uptake and inhibits the targeted endocytic degradation of the amino acid importer Slimfast. Thus, TOR simultaneously downregulates aspects of endocytosis that inhibit growth and up-regulates potential growth-promoting functions of endocytosis. In addition, we find that disruption of endocytosis leads to changes in TOR and phosphatidylinositol-3 kinase activity, affecting cell growth, autophagy, and rapamycin sensitivity. Our data indicate that endocytosis acts both as an effector function downstream of TOR and as a physiologically relevant regulator of TOR signaling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available