Multiple molecular mechanisms cause reproductive isolation between three yeast species.
Multiple molecular mechanisms cause reproductive isolation between three yeast species.
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DOI：
10.1371/journal.pbio.1000432
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发表时间：
2010-07-20
期刊：
影响因子：
9.8
通讯作者：
Leu JY
中科院分区：
文献类型：
--
作者：
Chou JY;Hung YS;Lin KH;Lee HY;Leu JY
在酵母物种的核和线粒体基因组之间的不相容性可能代表了在酵母进化过程中生殖隔离的一般机制。核-线粒体冲突（细胞核不相容性）是Dobzhansky-Muller不相容性的一种特殊形式，以前曾被证明会导致两种酵母菌的生殖隔离。本研究通过对三个近缘酵母属（S. Saccharomyces）的细胞核不亲和性引起的F2杂种不育性的系统研究，鉴定出两个新的不亲和基因MRS 1和AIM 22。酿酒酵母，S. paradoxus和S. bayanus）。Mrs 1是线粒体COX 1中剪接特异性内含子所需的核基因产物，Aim 22是线粒体蛋白脂酰化所需的核中编码的连接酶。通过比较不同物种，我们的结果表明，MRS 1的功能变化是共同进化的结果与COX 1内含子的变化。进一步的分子分析表明，三个非同义突变负责这些物种之间的Mrs 1的功能差异。功能互补分析，以确定这些不兼容的基因改变了他们的功能之间的强相关性的序列为基础的遗传学和细胞核不兼容性的演变。我们的研究结果表明，核-线粒体不相容性可能代表了酵母进化过程中生殖隔离的一般机制。物种之间的杂交通常是不能存活或不育的，可能是由于不同物种的基因之间的功能不相容。假设不相容的基因编码相互作用的成分，这些成分在与另一个物种的等位基因配对时无法正常发挥作用。为了了解不相容基因对如何导致杂种不育或不成活，重要的是要识别这些基因并重建它们的进化历史。先前的研究表明，核和线粒体基因组之间的不相容性（细胞核不相容性）导致两种酵母物种之间的杂交不育。为了扩展这些发现，我们筛选了三种酵母物种中涉及细胞核不相容性的基因，发现了两个核基因，MRS 1和AIM 22，它们编码的蛋白质不能支持杂交种中的完整线粒体功能。在这两个基因中，Mrs 1是去除线粒体COX 1基因中特定内含子所必需的。通过比较不同的酵母物种，我们发现一个明确的协同进化关系Mrs 1的功能和COX 1内含子模式。我们还表明，在Mrs 1 RNA结合结构域中的三个氨基酸的变化足以使Mrs 1在杂交种中不相容。我们的研究结果表明，细胞核的不相容性可能代表了一般机制的生殖隔离酵母进化过程中。
Incompatibility between nuclear and mitochondrial genomes in yeast species may represent a general mechanism of reproductive isolation during yeast evolution. Nuclear-mitochondrial conflict (cytonuclear incompatibility) is a specific form of Dobzhansky-Muller incompatibility previously shown to cause reproductive isolation in two yeast species. Here, we identified two new incompatible genes, MRS1 and AIM22, through a systematic study of F2 hybrid sterility caused by cytonuclear incompatibility in three closely related Saccharomyces species (S. cerevisiae, S. paradoxus, and S. bayanus). Mrs1 is a nuclear gene product required for splicing specific introns in the mitochondrial COX1, and Aim22 is a ligase encoded in the nucleus that is required for mitochondrial protein lipoylation. By comparing different species, our result suggests that the functional changes in MRS1 are a result of coevolution with changes in the COX1 introns. Further molecular analyses demonstrate that three nonsynonymous mutations are responsible for the functional differences of Mrs1 between these species. Functional complementation assays to determine when these incompatible genes altered their functions show a strong correlation between the sequence-based phylogeny and the evolution of cytonuclear incompatibility. Our results suggest that nuclear-mitochondrial incompatibility may represent a general mechanism of reproductive isolation during yeast evolution. Hybrids between species are usually inviable or sterile, possibly due to functional incompatibility between genes from the different species. Incompatible genes are hypothesized to encode interacting components that cannot function properly when paired with alleles from another species. To understand how incompatible gene pairs result in hybrid sterility or inviability, it is important to identify these genes and reconstruct their evolutionary history. A previous study has shown that incompatibility between nuclear and mitochondrial genomes (cytonuclear incompatibility) causes hybrid sterility between two yeast species. To expand on these findings, we screened three yeast species for genes involved in cytonuclear incompatibility, discovering two nuclear genes, MRS1 and AIM22, which encode proteins that are unable to support full mitochondrial function in the hybrids. Of these two genes, Mrs1 is required for removing a specific intron in the mitochondrial COX1 gene. By comparing different yeast species, we find a clear coevolutionary relationship between Mrs1 function and the COX1 intron pattern. We also show that changes in three amino acids in the Mrs1 RNA-binding domain are sufficient to make Mrs1 incompatible in hybrids. Our results suggest that cytonuclear incompatibility may represent a general mechanism of reproductive isolation during yeast evolution.
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影响因子：
3.3
作者：
Bolnick, Daniel I.;Turelli, Michael;Near, Thomas J.
通讯作者：
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影响因子：
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影响因子：
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作者：
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