ArticlePLoS genetics2012
The nucleoside diphosphate kinase gene Nme3 acts as quantitative trait locus promoting non-Mendelian inheritance.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Female- or male-biased offspring generated by targeted distortion of sex chromosome transmission in the mouse.Genetics · 2026Article
- The evolutionary genomics of meiotic drive.Molecular biology and evolution · 2026Article
- Acquisition of ampliconic sequences marks a selfish mouse t-haplotype.Nature communications · 2025Article
- Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024Review
- NME3 is a gatekeeper for DRP1-dependent mitophagy in hypoxia.Nature communications · 2024Article
- Bypassing Mendel's First Law: Transmission Ratio Distortion in Mammals.International journal of molecular sciences · 2023Review
- S. pombe wtf drivers use dual transcriptional regulation and selective protein exclusion from spores to cause meiotic drive.PLoS genetics · 2022Article
- Meiotic drive in house mice: mechanisms, consequences, and insights for human biology.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2022Review
- A meiotic driver alters sperm form and function in house mice: a possible example of spite.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2022Article
- Novel patterns of expression and recruitment of new genes on theProceedings. Biological sciences · 2022Article
- Mechanisms of meiotic drive in symmetric and asymmetric meiosis.Cellular and molecular life sciences : CMLS · 2021Review
- RAC1 controls progressive movement and competitiveness of mammalian spermatozoa.PLoS genetics · 2021Article
- TheeLife · 2020Article
- Recurrent breakdown and rebalance of segregation distortion in the genomes: battle for the transmission advantage.aBIOTECH · 2020Review
- Atypical meiosis can be adaptive in outcrossedeLife · 2020Article
- Dramatically diverse Schizosaccharomyces pombe wtf meiotic drivers all display high gamete-killing efficiency.PLoS genetics · 2020Article
- Effects of a male meiotic driver on male and female transcriptomes in the house mouse.Proceedings. Biological sciences · 2019Article
- Fertility Costs of Meiotic Drivers.Current biology : CB · 2019Review
- Two isoforms of the RAC-specific guanine nucleotide exchange factor TIAM2 act oppositely on transmission ratio distortion by the mouse t-haplotype.PLoS genetics · 2019Article
- A genetic system on chromosome arm 1BL of wild emmer causes distorted segregation in common wheat.Journal of genetics · 2018Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t-haplotype, a variant form of the t-complex region on mouse chromosome 17, acts as selfish genetic element and is transmitted at high frequencies (> 95%) from heterozygous (t/+) males to their offspring. This phenotype is termed transmission ratio distortion (TRD) and is caused by the interaction of the t-complex responder (Tcr) with several quantitative trait loci (QTL), the t-complex distorters (Tcd1 to Tcd4), all located within the t-haplotype region. Current data suggest that the distorters collectively impair motility of all sperm derived from t/+ males; t-sperm is rescued by the responder, whereas (+)-sperm remains partially dysfunctional. Recently we have identified two distorters as regulators of RHO small G proteins. Here we show that the nucleoside diphosphate kinase gene Nme3 acts as a QTL on TRD. Reduction of the Nme3 dosage by gene targeting of the wild-type allele enhanced the transmission rate of the t-haplotype and phenocopied distorter function. Genetic and biochemical analysis showed that the t-allele of Nme3 harbors a mutation (P89S) that compromises enzymatic activity of the protein and genetically acts as a hypomorph. Transgenic overexpression of the Nme3 t-allele reduced t-haplotype transmission, proving it to be a distorter. We propose that the NME3 protein interacts with RHO signaling cascades to impair sperm motility through hyperactivation of SMOK, the wild-type form of the responder. This deleterious effect of the distorters is counter-balanced by the responder, SMOK(Tcr), a dominant-negative protein kinase exclusively expressed in t-sperm, thus permitting selfish behaviour and preferential transmission of the t-haplotype. In addition, the previously reported association of NME family members with RHO signaling in somatic cell motility and metastasis, in conjunction with our data involving RHO signaling in sperm motility, suggests a functional conservation between mechanisms for motility control in somatic cells and spermatozoa.
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