2015 Fiscal Year Final Research Report
Analysis of A-type lamin functions in muscular development in Drosophila.
Project/Area Number |
25440081
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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 |
Cell biology
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Research Institution | Niigata University |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 筋肉 |
Outline of Final Research Achievements |
Functions of A-type lamin were analyzed because of knowing to cause various muscle dystrophies including cardiomyopathy. The loss of the A-type lamin gene in Drosophila resulted in pupal metamorphic lethality caused by tendon defects. In tendon cells lacking lamin C activity, overall cell morphology was affected and organization of the spectraplakin family cytoskeletal protein Short stop which is prominently expressed in tendon cells gradually disintegrated, notably around the nucleus and in a manner correlating well with the degradation of musculature. Furthermore, lamin C null mutants were efficiently rescued by restoring lamin C expression to shortstop-expressing cells, which include tendon cells but exclude skeletal muscle cells. Thus the critical function of A-type lamin C proteins in Drosophila musculature is to maintain proper function and morphology of tendon cells.
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Free Research Field |
発生生物学
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