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有害功能获得导致了水稻中的自身免疫反应和 Bateson-Dobzhansky-Muller 不兼容性。

Gain of deleterious function causes an autoimmune response and Bateson-Dobzhansky-Muller incompatibility in rice.

机构信息

Bioscience and Biotechnology Center, Nagoya University, Nagoya, 464-8601, Japan.

出版信息

Mol Genet Genomics. 2010 Apr;283(4):305-15. doi: 10.1007/s00438-010-0514-y. Epub 2010 Feb 6.

Abstract

Reproductive isolation plays an important role in speciation as it restricts gene flow and accelerates genetic divergence between formerly interbreeding population. In rice, hybrid breakdown is a common reproductive isolation observed in both intra and inter-specific crosses. It is a type of post-zygotic reproductive isolation in which sterility and weakness are manifested in the F(2) and later generations. In this study, the physiological and molecular basis of hybrid breakdown caused by two recessive genes, hbd2 and hbd3, in a cross between japonica variety, Koshihikari, and indica variety, Habataki, were investigated. Fine mapping of hbd2 resulted in the identification of the causal gene as casein kinase I (CKI1). Further analysis revealed that hbd2-CKI1 allele gains its deleterious function that causes the weakness phenotype by a change of one amino acid. As for the other gene, hbd3 was mapped to the NBS-LRR gene cluster region. It is the most common class of R-gene that triggers the immune signal in response to pathogen attack. Expression analysis of pathogen response marker genes suggested that weakness phenotype in this hybrid breakdown can be attributed to an autoimmune response. So far, this is the first evidence linking autoimmune response to post-zygotic isolation in rice. This finding provides a new insight in understanding the molecular and evolutionary mechanisms establishing post-zygotic isolation in plants.

摘要

生殖隔离在物种形成中起着重要作用,因为它限制了基因流动,并加速了曾经杂交的种群之间的遗传分化。在水稻中,杂种败育是在种内和种间杂交中都观察到的一种常见生殖隔离。它是一种合子后生殖隔离,其特征是在 F2 代和以后的世代中表现出不育和虚弱。在这项研究中,研究了隐性基因 hbd2 和 hbd3 引起的杂种败育的生理和分子基础,该杂种败育发生在粳稻品种越光(Koshihikari)和籼稻品种笹锦(Habataki)之间的杂交中。hbd2 的精细定位导致确定了致病基因是酪蛋白激酶 I (CKI1)。进一步的分析表明,hbd2-CKI1 等位基因通过一个氨基酸的变化获得了导致虚弱表型的有害功能。对于另一个基因 hbd3,它被定位到 NBS-LRR 基因簇区域。它是触发免疫信号以响应病原体攻击的最常见的 R 基因类。对病原体反应标记基因的表达分析表明,这种杂种败育的虚弱表型可归因于自身免疫反应。到目前为止,这是将自身免疫反应与水稻合子后隔离联系起来的第一个证据。这一发现为理解植物合子后隔离的分子和进化机制提供了新的认识。

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