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A knockout of ohe C. elegans folate transporter folt‐1 results in defective oocytes
Author(s) -
LaMunyon Craig Willis,
Liau WeiSiang,
Austin Misa,
Balamurugan Krishnaswamy,
Said Hamid
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.936.15
Subject(s) - sterility , biology , mutant , oocyte , genetics , somatic cell , embryo , oogenesis , gene , microbiology and biotechnology , spermatogenesis , caenorhabditis elegans , mutation , gene knockout , sperm , andrology , endocrinology , medicine
The C. elegans gene folt‐1 is an ortholog of the human reduced folate carrier gene. The FOLT‐1 protein has been shown to transport folate and to be involved in uptake of exogenous folate by worms. A knockout mutation of the gene, folt‐1(ok1460), was shown to cause sterility, and here we investigate the source of the sterility. Our results show that folt‐1(ok1460) worms are sterile due to defective oocytes. While the majority of mutant hermaphrodites are absolutely sterile, nearly 30% of the mutants produce a small brood numbering less than 10. All mutant hermaphrodites contained sperm, and their uteri harbored embryos with obvious defects. These defective embryos are rarely laid, indicating that oocyte production is limited. Supporting this conclusion, the proliferation of germ cells was drastically reduced in mutant hermaphrodites. folt‐1 males, however, proved fertile when paired with hermaphrodites, although not as fertile as wild‐type males. We conclude that oogenesis, and not spermatogenesis, is compromised in folt‐1(ok146) knockout mutant hermaphrodites, leading to reduction in oocyte production, defective embryos, and sterility. Therefore, FOLT‐1 must have a role in oocyte development and/or maturation. We also found that folt‐1 hermaphrodite lifespan is severely diminished, suggesting that FOLT‐1 has somatic functions as well, which supports the earlier findings that the protein is involved in uptake of exogenous folate.