Establishment of the Muscle-Tendon Junction During Thorax Morphogenesis in Drosophila Requires the Rho-Kinase
Author
dc.contributor.author
Vega Macaya, Franco
Author
dc.contributor.author
Manieu Seguel, Catalina
Author
dc.contributor.author
Valdivia, Mauricio
Author
dc.contributor.author
Mlodzik, Marek
Author
dc.contributor.author
Olguín Aguilera, Patricio
Admission date
dc.date.accessioned
2017-12-21T14:01:00Z
Available date
dc.date.available
2017-12-21T14:01:00Z
Publication date
dc.date.issued
2016
Cita de ítem
dc.identifier.citation
Genetics, Vol. 204, 1139–1149 November 2016
es_ES
Identifier
dc.identifier.issn
0016-6731
Identifier
dc.identifier.other
10.1534/genetics.116.189548
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/146242
Abstract
dc.description.abstract
The assembly of the musculoskeletal system in Drosophila relies on the integration of chemical and mechanical signaling between the developing muscles with ectodermal cells specialized as tendon cells. Mechanical tension generated at the junction of flight muscles and tendon cells of the notum epithelium is required for muscle morphogenesis, and is balanced by the epithelium in order to not deform. We report that Drosophila Rho kinase (DRok) is necessary in tendon cells to assemble stable myotendinous junctions (MTJ), which are required for muscle morphogenesis and survival. In addition, DRok is required in tendon cells to maintain epithelial shape and cell orientation in the notum, independently of chascon (chas). Loss of DRok function in tendon cells results in mis-orientation of tendon cell extensions and abnormal accumulation of Thrombospondin and beta PS-integrin, which may cause abnormal myotendinous junction formation and muscle morphogenesis. This role does not depend exclusively on nonmuscular Myosin-II activation (Myo-II), indicating that other DRok targets are key in this process. We propose that DRok function in tendon cells is key to promote the establishment of MTJ attachment and to balance mechanical tension generated at the MTJ by muscle compaction
es_ES
Patrocinador
dc.description.sponsorship
National Institutes of Health
GM-62917
FONDECYT
112053
Anillo
ACT-1401
Program U-Apoya (University of Chile)
Consejo Nacional de Ciencia y Technologia