Journal
FEBS JOURNAL
Volume 287, Issue 4, Pages 659-670Publisher
WILEY
DOI: 10.1111/febs.15039
Keywords
actin; Caenorhabditis elegans; genetics; immunoglobulin domain; sarcomere; striated muscle
Categories
Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- Natural Sciences and Engineering Research Council of Canada
- National Institutes of Health [AR48615]
Ask authors/readers for more resources
Among many essential genes in the nematode Caenorhabditis elegans, let-330 is located on the left arm of chromosome V and was identified as the largest target of a mutagen in this region. However, let-330 gene has not been characterized at the molecular level. Here, we report that two sequenced let-330 alleles are nonsense mutations of ketn-1, a previously characterized gene encoding kettin. Kettin is a large actin-binding protein of 472 kDa with 31 immunoglobulin domains and is expressed in muscle cells in C. elegans. let-330/ketn-1 mutants are homozygous lethal at the first larval stage with mild defects in body elongation. These mutants have severe defects in sarcomeric actin and myosin assembly in striated muscle. However, alpha-actinin and vinculin, which are components of the dense bodies anchoring actin to the membranes, were not significantly disorganized by let-330/ketn-1 mutation. Kettin localizes to embryonic myofibrils before alpha-actinin is expressed, and alpha-actinin deficiency does not affect kettin localization in larval muscle. Depletion of vinculin minimally affects kettin localization but significantly reduces colocalization of actin with kettin in embryonic muscle cells. These results indicate that kettin is an essential protein for sarcomeric assembly of actin filaments in muscle cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available