Deletion of lec-10, a galectin-encoding gene, increases susceptibility to oxidative stress in Caenorhabditis elegans.

ABSTRACT

Galectins are a family of beta-galactoside-binding lectins. They are involved in the regulation of a variety of biological phenomena in mammals. However, little is known about their roles in invertebrates. Caenorhabditis elegans is a well-characterized model organism whose complete genome has been sequenced. C. elegans is now being studied extensively in various fields of medical sciences. In this study, we examined the phenotypes of a mutant strain of C. elegans (tm1262) lacking lec-10, a galectin-encoding gene. We observed no difference in the rates of embryonic lethality and larval arrest/slow growth between this mutant strain and the wild-type strain. No apparent morphological defect was observed in the lec-10-deletion mutant (tm1262). Moreover, the life-spans of this mutant and the wild-type strain were equivalent. However, this mutant showed significantly greater susceptibility to paraquat and hydrogen peroxide than the wild type did. The lec-10-deletion mutants (tm1262) were as susceptible as the daf-16-deletion mutants (mu86) to paraquat and hydrogen peroxide. These results suggest that the deletion of lec-10 does not have a notable effect on the worm's survival under laboratory conditions. However, this study indicates that lec-10 does confer some protection against oxidative stress.