期刊
SCIENCE SIGNALING
卷 5, 期 243, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.2002802
关键词
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资金
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) [22300123, 23650200]
- Ministry of Health, Labour and Welfare (MHLW) [KHA1001, KHA1202, 24-18]
- Takeda Foundation
- Uehara Foundation
- Grants-in-Aid for Scientific Research [23650200, 22300123] Funding Source: KAKEN
Schwann cells respond to cues from axons by transforming their cellular morphology and forming myelin. We demonstrated that the guanine nucleotide exchange factor (GEF) cytohesin-1 promoted myelination by activating the small guanosine triphosphatase (GTPase) Arf6. In mice, ablating cytohesin-1 delayed myelination and diminished the amount of myelin produced. We determined that the Src-family kinase Fyn phosphorylated tyrosine 382 (Y-382) of cytohesin-1, and we generated transgenic mice that expressed a Schwann cell-specific phosphorylationmutant of cytohesin-1 (Y382F) that could not be targeted by Fyn. During development, these transgenic mice displayed delayed myelination compared to that of wild-type mice, as well as a decrease in the amount of myelin produced, similar to that observed in cytohesin-1(-/-) mice. These findings demonstrate that phosphorylation of cytohesin-1 by Fyn is required for full myelination and suggest that tyrosine phosphorylation of GEFs may be a mechanism to activate small GTPases engaged in cell morphogenesis.
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