Abstract:
:The unc-52 gene of Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecules, including EGL-17/FGF, UNC-129/TGF-beta, DBL-1/TGF-beta, and EGL-20/WNT. We propose that UNC-52 serves dual roles in C. elegans larval development in the maintenance of muscle structure and the regulation of growth factor-like signaling pathways.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Merz DC,Alves G,Kawano T,Zheng H,Culotti JGdoi
10.1016/s0012-1606(03)00014-9subject
Has Abstractpub_date
2003-04-01 00:00:00pages
173-86issue
1eissn
0012-1606issn
1095-564Xpii
S0012160603000149journal_volume
256pub_type
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