Hybridization has resulted in the origin and variation in extant species, and hybrids continue to arise despite pre- and post-zygotic barriers that limit their formation and evolutionary success. One important system that maintains species boundaries in prokaryotes and eukaryotes is the mismatch repair pathway, which blocks recombination between divergent DNA sequences. Previous studies illuminated the role of the mismatch repair component Msh2 in blocking genetic recombination between divergent DNA during meiosis. Loss of Msh2 results in increased interspecific genetic recombination in bacterial and yeast models, and increased viability of progeny derived from yeast hybrid crosses. Hybrid isolates of two pathogenic fungal Cryptococcus species, Cryptococcus neoformans and Cryptococcus deneoformans, are isolated regularly from both clinical and environmental sources. In the present study, we sought to determine if loss of Msh2 would relax the species boundary between C. neoformans and C. deneoformans. We found that crosses between these two species in which both parents lack Msh2 produced hybrid progeny with increased viability and high levels of aneuploidy. Whole-genome sequencing revealed few instances of recombination among hybrid progeny and did not identify increased levels of recombination in progeny derived from parents lacking Msh2. Several hybrid progeny produced structures associated with sexual reproduction when incubated alone on nutrient-rich medium in light, a novel phenotype in Cryptococcus. These findings represent a unique, unexpected case where rendering the mismatch repair system defective did not result in increased meiotic recombination across a species boundary. This suggests that alternative pathways or other mismatch repair components limit meiotic recombination between homeologous DNA and enforce species boundaries in the basidiomycete Cryptococcus species.

中文翻译：

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加强人类病原体新隐球菌和新隐球菌之间物种边界的因素

杂交已导致现存物种的起源和变异，尽管合子前和合子后障碍限制了它们的形成和进化成功，但杂种仍继续出现。维持原核生物和真核生物中物种边界的一个重要系统是错配修复途径，该途径阻止了不同DNA序列之间的重组。先前的研究阐明了错配修复组分Msh2在减数分裂过程中阻止发散DNA之间的基因重组的作用。Msh2的丢失会导致细菌和酵母模型中种间遗传重组的增加，以及源自酵母杂种杂交的子代的活力增加。两种病原性真菌隐球菌，新隐球菌和隐球菌是从临床和环境中定期分离得到的。在本研究中，我们试图确定的Msh2的损失将放松之间边界的品种隐球菌和C. deneoformans。我们发现，两个亲本都缺乏Msh2的物种之间的杂交产生了具有增强的活力和高水平非整倍性的杂交后代。全基因组测序揭示了杂交后代中很少有重组的实例，并且没有鉴定出源自缺乏Msh2的父母的后代中重组水平的提高。当在富含营养的培养基上单独孵育时，几种杂种后代产生与性繁殖相关的结构，这是隐球菌的一种新表型。这些发现代表了一个独特的，意想不到的情况，其中使失配修复系统产生缺陷并没有导致跨物种边界的减数分裂重组增加。这表明替代途径或其他错配修复成分限制了同源DNA之间的减数分裂重组，并增强了担子菌隐球菌物种中的物种边界。