The nematode Caenorhabditis elegans contains over 20 genes for TRP (transient receptor potential) channels which include members of all of the subclasses identified in mammalian cells. These proteins include three members of the TRPM (TRP melastatin) family: gon-2 (abnormal gonad development), gtl-1 (gon-2-like 1) and gtl-2. Although studies of these genes are at an early stage, we are beginning to understand their functions in the life of C. elegans. 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. Experiments on gon-2,gtl-1 double mutants show that they have a severe growth defect that is ameliorated by the addition of high levels of Mg(2+) to the growth medium. gon-2,gtl-1 double mutants have defective magnesium homoeostasis and also have altered sensitivity to toxic levels of Ni(2+). Furthermore gon-2 mutants have reduced levels of I(ORCa) (outwardly rectifying calcium current) in the intestinal cells. Thus these two channels appear to play an important role in cation homoeostasis in C. elegans. 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. The tractability of C. elegans as an experimental animal and its amenability to techniques such as RNAi (RNA interference) and in vivo imaging make it an excellent system for an integrative analysis of TRPM function.