2014 Fiscal Year Final Research Report
Role of transcription factor Elongin A with E3 activity in mouse neural development
Project/Area Number |
24590279
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General physiology
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Research Institution | Kochi University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | Elongin A / 転写伸長因子 / ユビキチンリガーゼ / 神経分化 / 発生 |
Outline of Final Research Achievements |
Elongin A increases the rate of RNA polymerase II (pol II) transcript elongation by suppressing transient pausing by the enzyme. Elongin A also acts as a component of E3 ubiquitin ligase that can target stalled pol II for ubiquitylation and proteasome- dependent degradation. The functions of Elongin A in vivo remain largely unclear. Recently we found that Elongin A-deficient (Elongin A-/-) mouse embryos exhibit abnormalities in the formation of both cranial and spinal nerves and that Elongin A-/- embryonic stem cells show a markedly decreased capacity to differentiate into neurons. Here we dementrated that Elongin A plays a critical role in the development of the sensory nervous system at least in part by regulating the differentiation processes of neural crest cells.
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Free Research Field |
分子生物学
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