|
pubmed:abstractText |
The gon-2 gene of Caenorhabditis elegans encodes a TRPM cation channel required for gonadal cell divisions. In this article, we demonstrate that the gonadogenesis defects of gon-2 loss-of-function mutants (including a null allele) can be suppressed by gain-of-function mutations in the gem-1 (gon-2 extragenic modifier) locus. gem-1 encodes a multipass transmembrane protein that is similar to SLC16 family monocarboxylate transporters. Inactivation of gem-1 enhances the gonadogenesis defects of gon-2 hypomorphic mutations, suggesting that these two genes probably act in parallel to promote gonadal cell divisions. GEM-1GFP is expressed within the gonadal precursor cells and localizes to the plasma membrane. Therefore, we propose that GEM-1 acts in parallel to the GON-2 channel to promote cation uptake within the developing gonad.
|
