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TRP (Transient Receptor Potential) cation channels of the TRPM subfamily have been found to be critically important for the regulation of Mg 2+  homeostasis in both protostomes (e.g., the nematode,  C .  elegans , and the insect,  D .  melanogaster ) and deuterostomes (e.g., humans). Although significant progress has been made toward understanding how the activities of these channels are regulated, there are still major gaps in our understanding of the potential regulatory roles of extensive, evolutionarily conserved, regions of these proteins. The  C .  elegans  genes,  gon-2 ,  gtl-1  and  gtl-2 , encode paralogous TRP cation channel proteins that are similar in sequence and function to human TRPM6 and TRPM7. We isolated fourteen revertants of the missense mutant,  gon-2(q338) , and these mutations affect nine different residues within GON-2. Since eight of the nine affected residues are situated within regions that have high similarity to human TRPM1,3,6 and 7, these mutations identify sections of these channels that are potentially critical for channel regulation. We also isolated a single mutant allele of  gon-2  during a screen for revertants of the Mg 2+ -hypersensitive phenotype of  gtl-2(-)  mutants. This allele of  gon-2  converts a serine to phenylalanine within the highly conserved TRP domain, and is antimorphic against both  gon-2(+)  and  gtl-1(+) . Interestingly, others have reported that mutation of the corresponding residue in TRPM7 to glutamate results in deregulated channel activity.

Novel Alleles of gon-2, a C. elegans Ortholog of Mammalian TRPM6 and TRPM7, Obtained by Genetic Reversion Screens