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2015 Fiscal Year Final Research Report

Analysis of A-type lamin functions in muscular development in Drosophila.

Research Project

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Project/Area Number 25440081
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Cell biology
Research InstitutionNiigata University

Principal Investigator

Kazuhiro Furukawa  新潟大学, 自然科学系, 教授 (40229109)

Project Period (FY) 2013-04-01 – 2016-03-31
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.

Free Research Field

発生生物学

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Published: 2017-05-10  

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