遗传
遺傳
유전
HEREDITAS(BEIJING)
2015年
2期
148-156
,共9页
范智权%孙加雷%单建伟%杨江义
範智權%孫加雷%單建偉%楊江義
범지권%손가뢰%단건위%양강의
偏分离%基因互作%广亲和%生殖隔离%杂种不育
偏分離%基因互作%廣親和%生殖隔離%雜種不育
편분리%기인호작%엄친화%생식격리%잡충불육
segregation distortion%gene interaction%wide compatibility%reproductive isolation%hybrid sterility
杂种偏分离是指杂交后代群体在某个位点的基因型分离比偏离了预期的孟德尔分离比例的一种现象,是来自不同杂交亲本基因之间的不兼容性所致。功能缺失型和功能获得型的基因间互作都可以导致杂种偏分离,其中前者的机理比较简单,即缺陷型的基因组合导致原有功能丧失而造成细胞死亡。功能获得型杂种偏分离系统是由多基因控制的遗传系统,包含两个基本成分:杀手(killer)因子和护卫(protector)因子,此外还有增强子(enhancer)、抑制基因(repressor)等修饰因子。功能获得型杂种偏分离有通用的遗传模型:具有传递优势的单倍型含有高活性的killer+和protector+;传递劣势的单倍型含有低活性的killer-和protector-;中性的单倍型(广亲和型)则含有 killer-和 protector+。该系统通过 killer 和 protector 间的紧密连锁、修饰因子的积累等途径得以在自然选择中保存下来。尽管不同功能获得型杂种偏分离系统的遗传机理有较高的相似性,但分子机制则大相径庭。文章综述了杂种偏分离的遗传和分子机理以及其与杂种不育的关系,以期为后续杂种偏分离研究提供参考。
雜種偏分離是指雜交後代群體在某箇位點的基因型分離比偏離瞭預期的孟德爾分離比例的一種現象,是來自不同雜交親本基因之間的不兼容性所緻。功能缺失型和功能穫得型的基因間互作都可以導緻雜種偏分離,其中前者的機理比較簡單,即缺陷型的基因組閤導緻原有功能喪失而造成細胞死亡。功能穫得型雜種偏分離繫統是由多基因控製的遺傳繫統,包含兩箇基本成分:殺手(killer)因子和護衛(protector)因子,此外還有增彊子(enhancer)、抑製基因(repressor)等脩飾因子。功能穫得型雜種偏分離有通用的遺傳模型:具有傳遞優勢的單倍型含有高活性的killer+和protector+;傳遞劣勢的單倍型含有低活性的killer-和protector-;中性的單倍型(廣親和型)則含有 killer-和 protector+。該繫統通過 killer 和 protector 間的緊密連鎖、脩飾因子的積纍等途徑得以在自然選擇中保存下來。儘管不同功能穫得型雜種偏分離繫統的遺傳機理有較高的相似性,但分子機製則大相徑庭。文章綜述瞭雜種偏分離的遺傳和分子機理以及其與雜種不育的關繫,以期為後續雜種偏分離研究提供參攷。
잡충편분리시지잡교후대군체재모개위점적기인형분리비편리료예기적맹덕이분리비례적일충현상,시래자불동잡교친본기인지간적불겸용성소치。공능결실형화공능획득형적기인간호작도가이도치잡충편분리,기중전자적궤리비교간단,즉결함형적기인조합도치원유공능상실이조성세포사망。공능획득형잡충편분리계통시유다기인공제적유전계통,포함량개기본성분:살수(killer)인자화호위(protector)인자,차외환유증강자(enhancer)、억제기인(repressor)등수식인자。공능획득형잡충편분리유통용적유전모형:구유전체우세적단배형함유고활성적killer+화protector+;전체열세적단배형함유저활성적killer-화protector-;중성적단배형(엄친화형)칙함유 killer-화 protector+。해계통통과 killer 화 protector 간적긴밀련쇄、수식인자적적루등도경득이재자연선택중보존하래。진관불동공능획득형잡충편분리계통적유전궤리유교고적상사성,단분자궤제칙대상경정。문장종술료잡충편분리적유전화분자궤리이급기여잡충불육적관계,이기위후속잡충편분리연구제공삼고。
Segregation distortion (SD) is defined as abnormal segregation ratio of hybrid offsprings at some ge-netic loci deviating from the Mendelian ratio. SD results from the incompatibility among genes from different parents, which could be due to loss-of-function or gain-of-function gene interactions. The mechanism for loss-of-function SD is relatively simple: defective gene combination leads to loss of the original function and eventual cell death. The gain-of-function hybrid SD system is a multi-gene genetic system, comprising two basic components: the killer and the protector. Additional modifiers, such as enhancers and repressors, are also involved. There is a general genetic model for gain-of-function hybrid SD:haplotypes with transmission advantage possess high-activity killer+and pro-tector+;those with transmission disadvantage possess low-activity killer-and protector-;neutral haplotypes (wide com-patibility types) possess killer-and protector+. Depending upon close linkage between the killer and the protector and the accumulation of modifiers, the SD system survived through natural selection. Although the genetic mechanisms are highly similar, different gain-of-function hybrid SD systems have distinctive molecular mechanisms. In this re-view, we summarize the genetic and molecular mechanisms of hybrid SD, and the relationship between hybrid SD and hybrid sterility.