ArticlePLoS genetics2016
Mg2+ Extrusion from Intestinal Epithelia by CNNM Proteins Is Essential for Gonadogenesis via AMPK-TORC1 Signaling in Caenorhabditis elegans.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Molecular bases of circadian magnesium rhythms across eukaryotes.FEBS letters · 2026Article
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- Lysosome Inhibition Reduces Basal and Nutrient-Induced Fat Accumulation inMolecules and cells · 2022Article
- Magnesium efflux from Drosophila Kenyon cells is critical for normal and diet-enhanced long-term memory.eLife · 2020Article
- Short-Term Mild Temperature-Stress-Induced Alterations in theInternational journal of molecular sciences · 2020Article
- PRL3 pseudophosphatase activity is necessary and sufficient to promote metastatic growth.The Journal of biological chemistry · 2020Article
- Stress and timing associated withHeliyon · 2020Article
- TOR Signaling inGenetics · 2019Review
- CrossTalk proposal: CNNM proteins are NaThe Journal of physiology · 2018Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mg2+ serves as an essential cofactor for numerous enzymes and its levels are tightly regulated by various Mg2+ transporters. Here, we analyzed Caenorhabditis elegans strains carrying mutations in genes encoding cyclin M (CNNM) Mg2+ transporters. We isolated inactivating mutants for each of the five Caenorhabditis elegans cnnm family genes, cnnm-1 through cnnm-5. cnnm-1; cnnm-3 double mutant worms showed various phenotypes, among which the sterile phenotype was rescued by supplementing the media with Mg2+. This sterility was caused by a gonadogenesis defect with severely attenuated proliferation of germ cells. Using this gonadogenesis defect as an indicator, we performed genome-wide RNAi screening, to search for genes associated with this phenotype. The results revealed that RNAi-mediated inactivation of several genes restores gonad elongation, including aak-2, which encodes the catalytic subunit of AMP-activated protein kinase (AMPK). We then generated triple mutant worms for cnnm-1; cnnm-3; aak-2 and confirmed that the aak-2 mutation also suppressed the defective gonadal elongation in cnnm-1; cnnm-3 mutant worms. AMPK is activated under low-energy conditions and plays a central role in regulating cellular metabolism to adapt to the energy status of cells. Thus, we provide genetic evidence linking Mg2+ homeostasis to energy metabolism via AMPK.
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