浅议水稻亚种间杂种不育性的遗传基础

水稻亚种间杂种不育性是一个普遍现象,但其遗传基础复杂。本文对这种亚种间杂种不育性的类型和表现,特别是前人推导两种解释杂种F1不育性遗传模型的研究方法、优越性及局限性进行了综述与分析,从中可以看出在水稻亚种间杂种F1不育性遗传研究上已经取得了较大的进展,在一些问题上已取得了一定的共识,如这种不育性的表现,细胞质的影响,杂交F1的染色体配对行为等;而在雌雄配子败育的作用大小,不育基因位点数目及不同不育基因位点的遗传特点等方面尚不完全一致;因而水稻亚种间杂种F1不育性的遗传有待进一步的研究。 Abstract：Hybrid sterility in the F1 populations of wide crosses in rice is a common phenomenon but the inheritance of the sterility is complex. This paper summarized the type and expression of the hybrid sterility, analyzed the experimental ideas, inference methods and advantage as well as disadvantages of two main genetic models used to explain the hybrid sterility, and concluded that there remains a lot to be investigated on the genetics of the hybrid sterility, for example, the number and effects of male and female sterility genes, although much advance has been made.     

水稻亚种间杂种是否存在雌性不育？

水稻亚种间杂种不育性是一种普遍现象,但其遗传基础复杂。目前在亚种间杂种不育遗传上,不同研究的结论不尽一致,即使对亚种间杂种不育性主要表现为雄性不育还是雌性不育也存在争论。本对证明水稻亚种间杂种存在和不存在雌性不育的研究进行了综述与分析。从中可以看出无论是认为水稻亚种间杂种不育性表现为雄性不育还是雌性不育的结论都有一定的片面性,尤其是Sano证明基因座S－5不存在的研究存在较大的缺陷。因此,水稻亚种间杂种雌雄配子败育对小穗育性影响的大小有待进一步研究。     

水稻亚种间杂种是否存在雌性不育?

水稻亚种间杂种不育性是一种普遍现象,但其遗传基础复杂.目前在亚种间杂种不育性遗传上,不同研究者的结论不尽一致,即使对亚种间杂种不育性主要表现为雄性不育还是雌性不育也存在争论.本文对证明水稻亚种间杂种存在和不存在雌性不育的研究进行了综述与分析,从中可以看出无论是认为水稻亚种间杂种不育性表现为雄性不育还是雌性不育的结论都有一定的片面性;尤其是Sano证明基因座S-5不存在的研究存在较大的缺陷.因此,水稻亚种间杂种雌雄配子败育对小穗育性影响的大小有待进一步研究。 Abstract:Hybrid sterility in the Fl populations of wide crosses in rice is a common phenomenon but the genetic basis of the sterility is complex.Whether male or female sterility is the main cause of the hybrid sterility remains controversial.This paper summarized the experiments which support or negate the existence of female sterility,analyzed the experimental ideas and inference methods of these experiments,especially Sano' s;and concluded that the conclusion that the hybrid sterility is only caused by male or female sterility is a one - sided view,therefore attention should be paid to the genetics of both female and male sterility.     

水稻广亲和性遗传的再研究

水稻广亲和基因的利用是克服亚种间杂种不育性的重要途径。但在广亲和性的遗传上不同研究者的结论不尽一致。以3种有广亲和品种参加的三交组合为研究材料,研究了品种Ketan Nangka的广亲和性遗传。结果表明水稻亚种杂交F1同时存在着雄性不育和雌性不育,但雄性不育对小穗育性的作用大小因组合而异;无论是在雄性不育位点还是雄性不育位点上,Ketan Nangka均具有相对应的中性基因（广亲和基因）;广亲和性的遗传特点与所用的籼粳测验品种间的杂种不育性密切相关;S－5位点的广亲和基因遗传符合单位点孢子体－配子体互作模型。     

不同倍性水稻亚种间杂种小孢子发生的细胞学观察

利用塑料半薄切片对水稻同源四倍体亚种间杂种F1及其对应的二倍体杂种F1小孢子母细胞减数分裂过程的细胞学变化进行观察研究.结果表明,同源四倍体水稻亚种间杂种造孢细胞期和小孢子母细胞期已经表现出较高频率的异常;减数分裂过程中,小孢子母细胞出现异常更加复杂,主要包括小孢子母细胞液泡化和退化两大类,这些异常是导致杂种花粉败育和花粉低育性的重要原因之一;此外,绒毡层异常也是导致杂种的花粉育性降低的因素.二倍体杂种小孢子母细胞在减数分裂过程的异常类型与水稻同源四倍体亚种间杂种基本相似,其绒毡层异常频率较低,对其花粉低育性影响不大.     

水稻籼粳杂种雌性不育的细胞学初步观察(简报)

普通栽培稻籼粳亚种间杂种结实率低是开展亚种间杂交育种和杂种优势利用的主要障碍。这一障碍是杂种花粉和胚囊的不育性引起的。不育性曾经认为是两者染色体在结构上存在微小的差异所致,但F_1植株减数分     

硅对水稻籼粳杂种雌雄配子育性和结实率的影响

以2个籼稻品种和2个粳稻品种及其籼粳杂种一代为材料,通过水培试验研究了硅对籼粳亚种间杂种雌雄配子育性和结实率的影响。结果表明:4个水稻亲本的育性正常,而亚种间杂种‘台中65’/‘广陆矮4号’和‘穞稻’/‘秋光’F1花粉育性分别为40.1%和50.3%,小穗育性分别为25.8%和40.3%;其F1胚囊具有正常的卵细胞、助细胞、极核及反足细胞,胚囊败育率分别为5.33%和3.33%。加硅处理F1每个柱头上花粉粒多于25粒的小花数分别占90%和90.5%,而不加硅处理高于20粒的小花数仅占8%和10%;加硅处理F1花粉离体萌发率分别为75.15%和76.23%,小穗的结实率分别达到65.5%和68.7%,而不加硅处理的分别为46.7%和48.13%,小穗结实率分别只有25.8%和40.3%,且加硅处理极显著高于不加硅处理。研究表明,水稻籼粳杂种存在半不育现象,并主要由花粉半不育和花药开裂性差造成;硅肥能促进杂种F1植株的花药开裂,明显增加柱头上花粉粒数目,并促进花粉萌发,显著提高小穗的结实率。     

水稻亚种间杂种小穗败育的细胞学基础

本文对普通栽培稻不同品种种类型间杂种小穗败育的细胞学基础及雌性败育的过程进行了研究,结果表明：（１）引起杂种小穗败育的原因有胚囊败育、花粉败育、开花时花药不开裂和雌雄异熟。其中胚囊败育而丧失受精能力是引起低结实率的最重要的因素,开花时花药不开裂和雌雄异熟在一定程度上形成了雌雄性细胞时间和空间的隔离屏障。     

单位点孢子体-配子体互作模型中不育基因的位置和效应的估计方法

水稻籼粳亚种间杂交F1通常表现为高度不育,这种不育性的一种遗传学解释称为单位点孢子体-配子体互作模型.为了研究这种不育性,提出了一种统计方法,可以估计单位点孢子体-配子体互作模型中不育基因位点的位置和效应.该方法利用回交群体中呈现异常分离的标记位点,用最大似然法对不育基因与标记位点之间的重组率和雌配子存活率进行估计.由于所依据的是非连续变异的遗传标记的分离,而不是连续分布的配子育性指标,因此可以避免由育性直接估计所带来的重组率结果的不稳定.     

克服棉花种间杂交不亲和性及杂种F_1不育性的试验效果

本世纪三十年代,许多遗传学家对棉花种间杂种的细胞学作了研究。四十年代对秋水仙精加倍技术的应用和五十年代杂种胚胎学的进一步研究都取得了较好的成果,为以后克服种间不亲和性和F_1不育性的系统研究打下了基础。 杂交组合中母本类型的选择,是早期取得的克服种间不亲和性的一项研究成果。中     

Genetics of hybrid male sterility among strains and species in the Drosophila pseudoobscura species group

Taxa in the early stages of speciation may bear intraspecific allelic variation at loci conferring barrier traits in hybrids such as hybrid sterility. Additionally, hybridization may spread alleles that confer barrier traits to other taxa. Historically, few studies examine within- and between-species variation at loci conferring reproductive isolation. Here, we test for allelic variation within Drosophila persimilis and within the Bogota subspecies of D. pseudoobscura at regions previously shown to contribute to hybrid male sterility. We also test whether D. persimilis and the USA subspecies of D. pseudoobscura share an allele conferring hybrid sterility in a D. pseudoobscura bogotana genetic background. All loci conferred similar hybrid sterility effects across all strains studied, although we detected some statistically significant quantitative effect variation among D. persimilis alleles of some hybrid incompatibility QTLs. We also detected allelism between D. persimilis and D. pseudoobscura USA at a second chromosome hybrid sterility QTL. We hypothesize that either the QTL is ancestral in D. persimilis and D. pseudoobscura USA and lost in D. pseudoobscura bogotana, or gene flow transferred the QTL from D. persimilis to D. pseudoobscura USA. We discuss our findings in the context of population features that may contribute to variation in hybrid incompatibilities.     

Haldane's rule: hybrid sterility affects the heterogametic sex first because sexual differentiation is on the path to species differentiation

Prevention of recombination is needed to preserve both phenotypic differentiation between species and sexual phenotypic differentiation within species. For species differentiation (speciation), isolating barriers preventing recombination may be pre-zygotic (gamete transfer barriers), or post-zygotic (either a developmental barrier resulting in hybrid inviability, or a chromosomal-pairing barrier resulting in hybrid sterility). The sterility barrier is usually the first to appear and, although often initially only manifest in the heterogametic sex (Haldane's rule), is finally manifest in both sexes. For sexual differentiation, the first and only barrier is chromosomal-pairing, and always applies to the heterogametic sex. For regions of sex chromosomes affecting sexual differentiation there must be something analogous to the process generating the hybrid sterility seen when allied species cross. Explanations for Haldane's rule have generally assumed that the chromosomal-pairing barrier initiating evolutionary divergence into species is due to incompatibilities between gene products ("genic), or sets of gene products ("polygenic), rather than between chromosomes per se ("chromosomal"). However, if chromosomal incompatibilities promoting incipient sexual differentiation could also contribute to the process of incipient speciation, then a step towards speciation would have been taken in the heterogametic sex. Thus, incipient speciation, manifest as hybrid sterility when "varieties" are crossed, would appear at the earliest stage in the heterogametic sex, even in genera with homomorphic sex chromosomes (Haldane's rule for hybrid sterility). In contrast, it has been proposed that Haldane's rule for hybrid inviability needs differences in dosage compensation, so could not apply to genera with homomorphic sex chromosomes.     

Comparative genetics of potential prezygotic and postzygotic isolating barriers in a Lycopersicon species cross

I compare the genetic basis of quantitative traits that potentially contribute to pre- and postzygotic isolation between the plant species Solanum lycopersicum (formerly Lycopersicon esculentum) and Solanum habrochaites (formerly Lycopersicon hirsutum), using quantitative trait loci (QTL) mapping in a set of near-isogenic lines. Putative prezygotic isolating traits include flower size, flower shape, stigma exertion, and inflorescence length, that can influence pollinator preferences and/or selfing rates, and therefore gene flow between divergent types. Postzygotic isolating traits are hybrid pollen and seed sterility. Three substantive results emerge from these analyses. First, the genetic basis of floral differentiation appears to be somewhat less complex than the genetic basis of postzygotic hybrid sterility, although these differences are very modest. Second, there is little evidence that traits for floral differentiation are causally or mechanistically associated with hybrid sterility traits in this species cross. Third, there is little evidence that hybrid sterility QTL are more frequently associated with chromosomal centromeric regions, in comparison to floral trait QTL, a prediction of centromeric drive models of hybrid sterility. Although genome-wide associations are not evident in this analysis, several individual chromosomal regions that contain clusters of QTL for both floral and sterility traits, or that indicate hybrid sterility effects at centromere locations, warrant further fine-scale investigation.     

Intraparental gamete competition provides a selective advantage for the development of hybrid sterility via meiotic drive

Hybrid sterility can have evolutionary significance and varies substantially by taxon, but few models attempt to predict or explain this variability. Hybrid sterility is commonly observed and develops early in isolation, at odds with straightforward models that predict it would develop slowly and rarely be seen. Meiotic drive might explain the rapid development of hybrid sterility, but drive is rarely observed, modifiers are expected to repress it, and no precise testable predictions are available. Here I develop population genetic models for the establishment of meiotic drive based on how it spreads by benefiting carrier gametes competing with noncarrier gametes from the same parent, or intraparental gamete competition. The resulting models predict that meiotic drive can often produce substantial hybrid sterility over time even in the presence of repressors, yet observable drive will be rare. They also make quantitative predictions of the degree of sterility based on observable parameters of reproductive ecology, including frequency of multiple mating, effective dispersal of offspring, and population size. Finally, they suggest explanations for the association of heterochromatin changes with speciation. Experimental evidence is discussed showing that drive alleles at least sometimes contribute to hybrid sterility.     

Complex epistasis and the genetic basis of hybrid sterility in the Drosophila pseudoobscura Bogota-USA hybridization.

We analyzed the genetic basis of postzygotic isolation between the Bogota and USA subspecies of Drosophila pseudoobscura. These subspecies diverged very recently (perhaps as recently as 155,000 to 230,000 years ago) and are partially reproductively isolated: Bogota and USA show very little prezygotic isolation but form sterile F1 males in one direction of the hybridization. We dissected the basis of this hybrid sterility and reached four main conclusions. First, postzygotic isolation appears to involve a modest number of genes: we found large chromosome regions that have no effect on hybrid fertility. Second, although apparently few in number, the factors causing hybrid sterility show a remarkably complex pattern of epistatic interaction. Hybrids suffer no hybrid sterility until they carry the "right" allele (Bogota vs. USA) at at least four loci. We describe the complete pattern of interactions between all chromosome regions known to affect hybrid fertility. Third, hybrid sterility is caused mainly by X-autosomal incompatibilities. Fourth, hybrid sterility does not involve a maternal effect, despite earlier claims to the contrary. In general, our results suggest that fewer genes are required for the appearance of hybrid sterility than implied by previous studies of older pairs of Drosophila species. Indeed, a maximum likelihood analysis suggests that roughly 15 hybrid male steriles separate the Bogota and USA subspecies. Only a subset of these would act in F1 hybrids.     

水稻的杂种不育研究进展

水稻亚种间杂种优势利用曾使水稻单产有了很大的提高,但水稻种间与亚种间的杂种不育性仍然普遍存在,从而影响了杂种优势的进一步利用。本研究对水稻产生杂种不育的细胞学水平原因进行了分类分析,对产生杂种不育的遗传学机理进行了探讨,对各种杂种不育基因座位的定位以及已克隆获得的基因进行了全面总结,并对如何克服杂交不育与利用杂种优势提出了自己的观点。     

The Genetics of Reproductive Isolation in the Drosophila Simulans Clade: X Vs. Autosomal Effects and Male Vs. Female Effects

A strong effect of homozygous autosomal regions on reproductive isolation was found for crosses between the species in the Drosophila simulans clade. Second chromosome regions were introgressed from D. mauritiana and D. sechellia into D. simulans and tested for their homozygous effects on hybrid male and hybrid female sterility and inviability. Most introgressions are fertile as heterozygotes, yet produce sterile male offspring when made homozygous. The density of homozygous autosomal factors contributing to hybrid male sterility is comparable to the density of X chromosome factors for this level of resolution. Female sterility was also revealed, yet the disparity between male and female levels of sterility was great, with male sterility being up to 23 times greater than female sterility. Complete hybrid inviability was also associated with some regions of the second chromosome, yet there were no strong sex differences. In conclusion, we find no evidence to support a strong X chromosome bias in the evolution of hybrid sterility or inviability but do find a very strong sex bias in the evolution of hybrid sterility. In light of these findings, we reevaluate the current models proposed to explain the genetic pattern of reproductive isolation.     

Mouse hybrid sterility and testicular function

Crosses of BALB/c female mice and inbred wild male mice (PWD, PWK) produce fertile female progeny, but the male offspring are sterile. The hybrid male sterility is a direct action of the hybrid sterility genes Hst-1s and Hstws. Previous reports concluded that spermatogenic arrest effected the sterility. However, the testicular steroidogenesis of hybrid sterile male mice has not been elucidated. In the present report, the steroidogenic capacity of hybrid sterile and parental strain males was directly assessed by quantifying testosterone secretion by maximally stimulated testes perfused in vitro. Additionally, Leydig cell mass and germ cell volumes were morphometrically determined. The experimental results confirm the deleterious impact of the Hst-1s/Hstws genotype on spermatogenesis and demonstrate for the first time that the steroidogenic capacity of hybrid sterile testes is reduced. The biochemical defects that cause the impairment of testicular function are unknown.     

Female sterility in hybrids between Anopheles gambiae and A. arabiensis, and the causes of Haldane's rule

Although F1 female hybrids between Anopheles gambiae and A. arabiensis are fully fertile, sterility is present in backcross females. Here we report the results of a study into the genetic basis of backcross female sterility. Using 23 markers, we performed quantitative trait loci (QTL) mapping analyses to identify chromosomal regions involved in hybrid female sterility. We found that female sterility in backcrosses in both directions is primarily caused by interspecific interactions between a heterozygous X chromosome and recessive autosomal factors. In addition, our data provide support for two theories implicated in Haldane's rule in a single taxon. A comparison with data from a previous study shows that male hybrid sterility QTL are present in higher numbers than female hybrid sterility QTL. Furthermore, autosomal female sterility factors tend to be recessive, supporting the dominance theory for female sterility. Finally, our data indicate a very large effect of the X chromosome from both species on hybrid female sterility, despite the fact that the X chromosome represents less than 9% of the genome. However, this could be the result of a lack of introgression of the X chromosome between A. gambiae and A. arabiensis, rather than a faster evolution of sterility factors on the X chromosome.     

Vitellogenetic defects in hybrids of the species pair Drosophila virilis and Drosophila texana

In interspecific matings between the species Drosophila virilis and Drosophila texana, female sterility can be observed in F₂ backcross females and in F₂ hybrid females. The results presented in this report show that the female sterility, whenever it exists, is due to prevention of vitellogenin synthesis in the fat body, but other abnormalities such as defects with the hybrid ovaries are not excluded. The observation that sterility appears among females from backcrosses suggests that incompatibilities between interspecific genes may cause female sterility even in the presence of a complete habloid genome from one or the other species. Yet, the parallel observation that female sterility appears only in hybrid females with recombinant chromosomes indicates that sterility results when conspecific combinations of genes on the same chromosome are broken by interspecific recombination. © 1996 Wiley-Liss, Inc.