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In previous work, we found that gain-of-function mutations that hyperactivate GEM-1 (an SLC16A transporter protein) can bypass the requirement for GON-2 (a TRPM channel protein) during the initiation of gonadogenesis in  C. elegans . Consequently, we proposed that GEM-1 might function as part of a Mg 2+  uptake pathway that functions in parallel to GON-2. In this study, we report that CATP-6, a  C. elegans  ortholog of the P5B ATPase, ATP13A2 (PARK9), is necessary for  gem-1  gain-of-function mutations to suppress the effects of  gon-2  inactivation. One possible explanation for this observation is that GEM-1 serves to activate CATP-6, which then functions as a Mg 2+  transporter. However, we found that overexpression of GEM-1 can alleviate the requirement for CATP-6 activity, suggesting that CATP-6 probably acts as a non-essential upstream positive regulator of GEM-1. Our results are consistent with the notion that P5B ATPases govern intracellular levels of Mg 2+  and/or Mn 2+  by regulating the trafficking of transporters and other proteins associated with the plasma membrane.

CATP-6, a C. elegans Ortholog of ATP13A2 PARK9, Positively Regulates GEM-1, an SLC16A Transporter