Mechanisms of expression and translocation of major fission yeast glucose transporters regulated by CaMKK/phosphatases, nuclear shuttling, and TOR
| Autor: | Lisa Uehara, Ayaka Mori, Mitsuhiro Yanagida, Fumie Masuda, Shigeaki Saitoh, Saeko Soejima |
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| Rok vydání: | 2015 |
| Předmět: |
Snf3
Monosaccharide Transport Proteins Fission Green Fluorescent Proteins Immunoblotting Phosphatase Active Transport Cell Nucleus Glucose Transport Proteins Facilitative Calcium-Calmodulin-Dependent Protein Kinase Kinase Cell Cycle Proteins Chromosomal translocation Mechanistic Target of Rapamycin Complex 2 Biology Time-Lapse Imaging Transcription (biology) Gene Expression Regulation Fungal Schizosaccharomyces Phosphoprotein Phosphatases Humans Protein Isoforms Glucose homeostasis HSP70 Heat-Shock Proteins Molecular Biology Cell Nucleus TOR Serine-Threonine Kinases Glucose transporter Articles Cell Biology Signaling Yeast Cell biology Glucose Microscopy Fluorescence Biochemistry Multiprotein Complexes Mutation Schizosaccharomyces pombe Proteins |
| Zdroj: | Molecular Biology of the Cell |
| ISSN: | 1939-4586 1059-1524 |
| DOI: | 10.1091/mbc.e14-11-1503 |
| Popis: | Glucose transporters play a pivotal role in glucose homeostasis. The fission yeast high-affinity glucose transporter Ght5 is regulated with regard to transcription and localization via CaMKK and TOR pathways. These results clarify the evolutionarily conserved mechanisms underlying glucose homeostasis that prevent hyperglycemia in humans. Hexose transporters are required for cellular glucose uptake; thus they play a pivotal role in glucose homeostasis in multicellular organisms. Using fission yeast, we explored hexose transporter regulation in response to extracellular glucose concentrations. The high-affinity transporter Ght5 is regulated with regard to transcription and localization, much like the human GLUT transporters, which are implicated in diabetes. When restricted to a glucose concentration equivalent to that of human blood, the fission yeast transcriptional regulator Scr1, which represses Ght5 transcription in the presence of high glucose, is displaced from the nucleus. Its displacement is dependent on Ca2+/calmodulin-dependent kinase kinase, Ssp1, and Sds23 inhibition of PP2A/PP6-like protein phosphatases. Newly synthesized Ght5 locates preferentially at the cell tips with the aid of the target of rapamycin (TOR) complex 2 signaling. These results clarify the evolutionarily conserved molecular mechanisms underlying glucose homeostasis, which are essential for preventing hyperglycemia in humans. |
| Databáze: | OpenAIRE |
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