ArticlePLoS genetics2011
A mutation in the gene encoding mitochondrial Mg²+ channel MRS2 results in demyelination in the rat.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- Expression and distribution of tribbles pseudokinase 3 in oxidative stress-mediated acute liver and kidney injury models.Journal of toxicologic pathology · 2026Article
- Structure and function of the human mitochondrial MRS2 channel.Nature structural & molecular biology · 2025Article
- Mitochondrial translation failure represses cholesterol gene expression via Pyk2-Gsk3β-Srebp2 axis.Life science alliance · 2024Article
- Neuroprotective effects of magnesium: implications for neuroinflammation and cognitive decline.Frontiers in endocrinology · 2024Review
- A missense mutation in theFrontiers in neuroscience · 2024Article
- Acute Necrotizing Encephalopathy in Children: Insights and Outcomes from Iran.Iranian journal of child neurology · 2024Article
- Cryo-EM structures of human magnesium channel MRS2 reveal gating and regulatory mechanisms.Nature communications · 2023Article
- Importance of Magnesium Status in COVID-19.Biology · 2023Review
- Positional cloning of rat mutant genes reveals new functions of these genes.Experimental animals · 2023Review
- Ion selectivity and gating behavior of the CorA-type channel Bpss1228.Frontiers in chemistry · 2022Article
- Mitochondrial Metal Ion Transport in Cell Metabolism and Disease.International journal of molecular sciences · 2021Review
- Magnesium, Little Known But Possibly Relevant: A Link between NASH and Related Comorbidities.Biomedicines · 2021Review
- Deficiency of the RIβ subunit of protein kinase A causes body tremor and impaired fear conditioning memory in rats.Scientific reports · 2021Article
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- Magnesium Is a Key Player in Neuronal Maturation and Neuropathology.International journal of molecular sciences · 2019Review
- Inherited and acquired disorders of myelin: The underlying myelin pathology.Experimental neurology · 2016Review
- Involvement of aspartoacylase in tremor expression in rats.Experimental animals · 2016Article
- Mitochondrial Mg(2+) homeostasis decides cellular energy metabolism and vulnerability to stress.Scientific reports · 2016Article
- Solute carrier 41A3 encodes for a mitochondrial Mg(2+) efflux system.Scientific reports · 2016Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rat demyelination (dmy) mutation serves as a unique model system to investigate the maintenance of myelin, because it provokes severe myelin breakdown in the central nervous system (CNS) after normal postnatal completion of myelination. Here, we report the molecular characterization of this mutation and discuss the possible pathomechanisms underlying demyelination. By positional cloning, we found that a G-to-A transition, 177 bp downstream of exon 3 of the Mrs2 (MRS2 magnesium homeostasis factor (Saccharomyces cerevisiae)) gene, generated a novel splice acceptor site which resulted in functional inactivation of the mutant allele. Transgenic rescue with wild-type Mrs2-cDNA validated our findings. Mrs2 encodes an essential component of the major Mg²+ influx system in mitochondria of yeast as well as human cells. We showed that the dmy/dmy rats have major mitochondrial deficits with a markedly elevated lactic acid concentration in the cerebrospinal fluid, a 60% reduction in ATP, and increased numbers of mitochondria in the swollen cytoplasm of oligodendrocytes. MRS2-GFP recombinant BAC transgenic rats showed that MRS2 was dominantly expressed in neurons rather than oligodendrocytes and was ultrastructurally observed in the inner membrane of mitochondria. Our observations led to the conclusion that dmy/dmy rats suffer from a mitochondrial disease and that the maintenance of myelin has a different mechanism from its initial production. They also established that Mg²+ homeostasis in CNS mitochondria is essential for the maintenance of myelin.
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