High impact information on gon-2

• The initiation of postembryonic cell divisions by the gonadal precursors of C. elegans requires the activity of gon-2. gon-2 encodes a predicted cation channel (GON-2) of the TRPM subfamily of TRP proteins and is likely to mediate the influx of Ca(2+) and/or Mg(2+) [1].
• In gon-2 mutants, gonadogenesis is severely impaired; in some animals, none of the gonad progenitors undergo any postembryonic divisions [2].
• The results of upshift experiments using a temperature-sensitive allele suggest that zygotic expression of gon-2 begins early in embryogenesis, before the birth of Z1 and Z4 [2].
• By cell lineage analysis, we found that the priman, defect in gon-2 mutants is a delay (sometimes a complete block) in the onset and continuation of gonadal divisions [2].
• The C. elegans gon-2 gene encodes a putative TRP cation channel protein required for mitotic cell cycle progression [3].

Biological context of gon-2

• Mutations in gon-2 have defective gonad formation because of failures in the cell division of the somatic gonad precursor cells. gon-2 and gtl-1 are both expressed in the intestine of the animal [4].
• In addition, perturbing the function of gon-2 and gtl-1 disrupts the ultradian defecation rhythm in C. elegans, suggesting that these channels play an important role in regulating this calcium-dependent rhythmic process [4].

References