Knockout of the folate transporter folt-1 causes germline and somatic defects in C. elegans
1 Department of Biological Sciences, California State University Pomona, CA 91768, USA
2 Current Address: Department of Chemistry and Biochemistry, University of California, Los Angeles, CA 90095, USA
3 Veterans Affairs Medical Center, Long Beach, CA 90822, USA
4 Departments of Medicine and Physiology/Biophysics, University of California, Irvine, CA 92697, USA
5 Current Address: Department of Biotechnology, Alagappa University, Karaikudi 630 003, India
BMC Developmental Biology 2010, 10:46 doi:10.1186/1471-213X-10-46Published: 4 May 2010
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 and the effect of the folt-1 knockout on somatic function.
Our results show that folt-1(ok1460) knockout hermaphrodites have a substantially reduced germline, generate a small number of functional sperm, and only rarely produce a functional oocyte. We found no evidence of increased apoptosis in the germline of folt-1 knockout mutants, suggesting that germline proliferation is defective. While folt-1 knockout males are fertile, their rate of spermatogenesis was severely diminished, and the males were very poor maters. The mating defect is likely due to compromised metabolism and/or other somatic functions, as folt-1 knockout hermaphrodites displayed a shortened lifespan and elongated defecation intervals.
The FOLT-1 protein function affects both the soma and the germline. folt-1(ok1460) hermaphrodites suffer severely diminished lifespan and germline defects that result in sterility. Germline defects associated with folate deficiency appear widespread in animals, being found in humans, mice, fruit flies, and here, nematodes.