Open AccessFGT‐1‐mediated glucose uptake is defective in insulin/IGF‐like signaling mutants in Caenorhabditis elegans
Author(s) -
Kitaoka Shun,
Morielli Anthony D.,
Zhao FengQi
Publication year - 2016
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12068
Subject(s) - caenorhabditis elegans , mutant , insulin , biology , glucose transporter , insulin receptor , microbiology and biotechnology , function (biology) , signal transduction , biochemistry , gene , endocrinology , insulin resistance
Insulin signaling plays a central role in the regulation of facilitative glucose transporters (GLUTs) in humans. To establish Caenorhabditis elegans ( C. elegans ) as a model to study the mechanism underlying insulin regulation of GLUT, we identified that FGT‐1 is most likely the only functional GLUT homolog in C. elegans and is ubiquitously expressed. The FGT‐1‐mediated glucose uptake was almost completely defective in insulin/IGF‐like signaling (IIS) mutants daf‐2 and age‐1 , and this defect mainly resulted from the down‐regulated FGT‐1 protein expression. However, glycosylation may also be involved because OGA‐1, an O ‐GlcNAcase, was essential for the function of FGT‐1. Thus, our study showed that C. elegans can be a new powerful model system to study insulin regulation of GLUT.