| Literature DB >> 14597206 |
Vera Hapiak1, Michelle Coutu Hresko, Lawrence A Schriefer, Kamlai Saiyasisongkhram, Mark Bercher, John Plenefisch.
Abstract
Locomotion in Caenorhabditis elegans requires force transmission through a network of proteins linking the skeletal muscle, via an intervening basal lamina and epidermis (hypodermis), to the cuticle. Mutations in mua-6 result in hypodermal rupture, muscle detachment from the bodywall, and progressive paralysis. It is shown that mua-6 encodes the cytoplasmic intermediate filament (cIF) A2 protein and that a MUA-6/IFA-2::GFP fusion protein that rescues the presumptive mua-6 null allele localizes to hypodermal hemidesmosomes. This result is consistent with what is known about the function of cIFs in vertebrates. Although MUA-6/IFA-2 is expressed embryonically, and plays an essential postembryonic role in tissue integrity, it is not required for embryonic development of muscle-cuticle linkages nor for the localization of other cIFs or hemidesmosome-associated proteins in the embryo. Finally, the molecular lesion in the mua-6(rh85) allele suggests that the head domain of the MUA-6/IFA-2 is dispensable for its function.Entities:
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Year: 2003 PMID: 14597206 DOI: 10.1016/j.ydbio.2003.08.001
Source DB: PubMed Journal: Dev Biol ISSN: 0012-1606 Impact factor: 3.582