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A Multi-Megabase Copy Number Gain Causes Maternal Transmission Ratio Distortion on Mouse Chromosome 2
One of the strongest expectations in genetics is that chromosomes segregate randomly during meiosis. However, genetic loci that exhibit transmission ratio distortion (TRD) are sometimes observed in offspring of F1 hybrids. Meiotic drive is a type of non-Mendelian inheritance in which a “selfish” genetic element exploits asymmetric female meiotic cell division to promote its preferential inclusion in ova. We previously reported TRD on Chr 2 in the CC, a mouse recombinant inbred panel with contributions from three Mus musculus subspecies. Here we show that maternal TRD consistent with a novel meiotic drive system is caused by a copy number gain. This mutation is similar in size and structure to other known meiotic drive responders, such as the knobs of maize. A deletion of most of the copies is sufficient to restore Mendelian segregation, proving that the copy number variant is causative of the observed TRD. In the CC, and also the related DO population, the transmission frequency of the favored allele varies dependent on genetic background, demonstrating that this system is under genetic control. In conclusion, we describe a novel wild-derived meiotic drive locus on mouse Chr 2 that exploits female meiosis asymmetry to violate the Laws of Mendelian inheritance.
Vyšlo v časopise: A Multi-Megabase Copy Number Gain Causes Maternal Transmission Ratio Distortion on Mouse Chromosome 2. PLoS Genet 11(2): e32767. doi:10.1371/journal.pgen.1004850
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004850Souhrn
One of the strongest expectations in genetics is that chromosomes segregate randomly during meiosis. However, genetic loci that exhibit transmission ratio distortion (TRD) are sometimes observed in offspring of F1 hybrids. Meiotic drive is a type of non-Mendelian inheritance in which a “selfish” genetic element exploits asymmetric female meiotic cell division to promote its preferential inclusion in ova. We previously reported TRD on Chr 2 in the CC, a mouse recombinant inbred panel with contributions from three Mus musculus subspecies. Here we show that maternal TRD consistent with a novel meiotic drive system is caused by a copy number gain. This mutation is similar in size and structure to other known meiotic drive responders, such as the knobs of maize. A deletion of most of the copies is sufficient to restore Mendelian segregation, proving that the copy number variant is causative of the observed TRD. In the CC, and also the related DO population, the transmission frequency of the favored allele varies dependent on genetic background, demonstrating that this system is under genetic control. In conclusion, we describe a novel wild-derived meiotic drive locus on mouse Chr 2 that exploits female meiosis asymmetry to violate the Laws of Mendelian inheritance.
Zdroje
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