Probable metal transporter. Probably acts redundantly with the other metal transport proteins cnnm-1, cnnm-2, cnnm-4 and cnnm-5 to regulate Mg(2+) homeostasis. Promotes postembryonic gonad development by regulating Mg(2+) levels, probably via AMPK signaling. Highly expressed in the intestine and in neurons, but it is also expressed in a variety of tissues including the pharynx, hypodermis, rectum and in muscles. No visible phenotype. Double knockout with cnnm-1 results in increased levels of intestinal Mg(2+) and reduced levels in other tissues. This Mg(2+) deficiency in tissues leads to a reduced lifespan, 100% sterility, and smaller animals that exhibit a developmental delay with defective gonad development and which therefore do not produce oocytes or form vulva. In addition, the gonad development defect in the cnnm-1 and cnnm-3 double knockout is rescued when the AMPK alpha subunit aak-2 is also knocked out. Double knockout with cnnm-2 results in 22% sterility. Quintuple knockout with cnnm-1, cnnm-2, cnnm-4 and cnnm-5 results in a reduced lifespan and 100% sterility. Belongs to the ACDP family.