To unlock all 5, videos, start your free trial. Reproductive isolation is a mechanism that keeps species from mating with others. Prezygotic isolation prevents the fertilization of eggs while postzygotic isolation prevents the formation of fertile offspring.
Prezygotic mechanisms include habitat isolation, mating seasons, "mechanical" isolation, gamete isolation and behavioral isolation. Postzygotic mechanisms include hybrid inviability, hybrid sterility and hybrid "breakdown. In evolution, one of the major concepts is what is a species? And a species is a group of organisms that are reproductively isolated from each other. Now, what does that mean? Well, reproductive isolation depends on various mechanisms that keep one species from being able to succesfully mate with other species.
Now these fall into two categories, these reproductive isolating mechanisms. They're are pre-zygotic reproductive isolating mechanisms, the ones that prevents the zygote from happening the fertilization of the egg by sperm. As compared to the post zygotic reproductive isolating mechanisms. Those are okay, we got the sperm to the egg.
This is what prevents the formation of a fertile viable hybrid offspring. And just in case I didn't say it before, hybrid is a cross between two different species. Now pre-zygotic reproductive isolating mechanisms fall into several different categories. There is habitat isolation. If the two species live in different locations and their habitats never coincide, that will keep them isolated, this is one of the reasons why we consider lions and tigers to be two separate species even though, some of you that have paid attention to some of the freakier parts of your text book may have seen pictures of ligers or tiglons.
Because, if you have a really artificial situation, you have a zoo. And somebody happens to keep the tigers and lions in the same cage or in close enough cages, sometimes in a weirdly different situation you can wind up with tigers and lions successfully mating with each other and producing this tiglon or liger. Mating seasons or sometimes they'll call it temporal isolation. If your mating season is say the spring, then you wil mate with your species during the spring.
You will not mate with the species whose mating season is say the fall. You walk up to them, "you don't want to mate? They're completely disinterested. Meanwhile, fall comes around, they come up to you. Not the time for it.
So that's another way of keeping two perhaps closely related species separate from each other. Mechanical isolation. I'll put that in quotes and I'll put some other things into quotes. This is when the mechanics prevent it. Essentially when the male key doesn't fit the female's lock. To explain the surprising result that epistasis among three alleles is required for abortion of japonica SaM -carrying microspores, the authors propose a complicated model in which indica -encoded SaM and SaF proteins are transported between haploid microspores during early pollen development to kill gametes that inherit the japonica SaM allele [ 40 ].
The idea is that the japonica SaM protein is unable to move between microspores, so pollen grains that carry indica alleles at SaM and SaF — but do not receive the interacting japonica SaM protein — remain viable.
An important, unanswered question is what caused the japonica haplotype to become fixed. A classic, single-locus incompatibility between Oryza sativa indica and Oryza sativa japonica is conferred by two adjacent genes depicted here as striped and solid. Semi-sterility occurs in F 1 hybrids that carry blue alleles at the striped and solid genes indica haplotype in combination with a green allele at the solid gene japonica haplotype. Figure adapted from [ 40 ]. In the third case, Zhao et al.
Like S5 and Sa , the SEFS hybrid incompatibility is a gain-of-function: pollen grains with japonica S24 alleles are aborted in S24 -heterozygotes, but only when the plant is also homozygous for japonica alleles at EFS. As with Sa , it is possible that the otherwise deleterious japonica S24 allele was only able to spread in a permissive, indica -like EFS background, but the necessary phylogeographic analyses have not yet been done.
It is also worth noting that for both Sa and S24 , certain wide compatibility varieties carry neutral alleles that rescue pollen sterility [ 43 , 45 ], indicating that the evolutionary histories of these incompatibilities might include alternate mutational routes.
This conclusion flows rather easily from those cases in which hybrid dysfunction is caused by epistasis between two or more unlinked genes, but it has been less obvious for a number of classic, single-locus incompatibilities [ 31 ]. Because of several recent detailed genetic studies, however, we now know that even these single-locus incompatibilities arose by mutations in two tightly linked genes, or, at the very least, two or more amino acid changes encoded within the same gene.
Thus, it is possible that most of these incompatibility alleles appeared without any reductions in fitness within species. Of course, the key question for speciation is which evolutionary forces allow incompatibility alleles to increase in frequency and eventually become fixed within species. For a few of the cases discussed above there is evidence that natural selection e. It also appears that there are some common genetic routes to plant hybrid dysfunction.
Indeed, immune system genes seem to contribute disproportionately to hybrid necrosis. As we have seen, it is even possible for the very same gene to be involved in multiple cases of hybrid dysfunction: divergent duplicate loci carry a striking number of independently derived, loss-of-function mutations.
Yet, there are many hybrid incompatibilities that do not involve disease resistance or duplicate genes, and, for these systems, we are only beginning to understand the evolutionary causes of divergence. Remarkably, at least 50 loci contribute to hybrid sterility between the closely related subspecies Oryza sativa indica and Oryza sativa japonica [ 46 ]. So does this large number reflect a special propensity in rice species for evolving hybrid sterility?
Although our current sample of plant hybrid incompatibility genes comes from only two genera Oryza and Arabidopsis , there are a number of classic [ 46 , 47 ] and more recently identified [ 48 - 51 ] incompatibility systems that are not yet molecularly defined. As advances in genomics and DNA sequencing technologies enable rigorous genetic analysis of reproductive isolation in a number of emerging model systems, we should gain new insight into which factors affect the number and nature of hybrid incompatibilities that accumulate between plant species.
National Center for Biotechnology Information , U. Journal List F Biol Rep v. F Biol Rep. Published online Dec 3. Andrea L. Sweigart 1 and John H. Willis 2. John H. Author information Copyright and License information Disclaimer. Corresponding author. Sweigart: ude. Willis: ude. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
You may not use this work for commercial purposes. This article has been cited by other articles in PMC. Abstract In just the last few years, plant geneticists have made tremendous progress in identifying the molecular genetic basis of postzygotic reproductive isolation. Introduction The goal of explaining the origin of species has inspired more than two centuries of scientific inquiry, involving early naturalists through to modern evolutionary biologists.
The Dobzhansky-Muller model Dobzhansky [ 6 ] and Muller [ 7 ] outlined a solution to this puzzle, explaining that if postzygotic isolation is caused by incompatible gene interactions between diverging species then natural selection need not oppose its evolution. Recent advances Two-locus hybrid incompatibilities In the classic model of speciation, hybrid incompatibilities are thought to evolve as a by-product of adaptation to different environments [ 13 ].
Single-locus hybrid incompatibilities In addition to the cases described above, studies have occasionally discovered hybrid incompatibilities that map to single genetic loci [ 31 , 32 ], which might be taken as prima facie evidence that postzygotic isolation can evolve via a single mutational step.
Open in a separate window. Figure 1. The Dobzhansky-Muller model for a single-locus hybrid incompatibility An ancestral population splits into two geographically isolated populations that diverge genetically and eventually fix different alleles red or blue at the same locus.
Figure 2. Model for the evolution of Sa hybrid sterility in rice A classic, single-locus incompatibility between Oryza sativa indica and Oryza sativa japonica is conferred by two adjacent genes depicted here as striped and solid. Conclusions and future challenges In just the last few years, plant geneticists have made tremendous progress in identifying the molecular genetic basis of postzygotic reproductive isolation.
Notes Competing interests The authors declare that they have no competing interests. References 1. Darwin C. On the Origin of Species. Murray; London: Mayr E. Systematics and the Origin of Species. Columbia University Press; New York: Schluter D, Conte GL.
Genetics and ecological speciation. Sinauer; Sunderland, Massachusetts: The biology of speciation. Dobzhansky T H. Genetics and the Origin of Species. Muller HJ. Isolating mechanisms, evolution, and temperature. Biol Symp. Plant speciation. Cloning and sequencing studies revealed that loss-of-function mutations of duplicate genes cause functional defects in male gametes in rice Mizuta et al. Potentially plant F 1 hybrid incompatibility could be explained by simple genetic mechanisms involving a small number of loci, such as one-locus allelic interactions or duplicate genes.
However, the studies cited above indicate that both genetic models include epistasis-related effects among multiple linked or unlinked loci. It is expected that diversified forms of epistatic interactions will be revealed by future cloning studies of additional F 1 sterility genes. The three F 1 sterility genes, S24 , S25 and S35 , cause developmental defects at mitotic stages of male gametogenesis Kubo et al.
Interestingly, other rice F 1 sterility genes tend to evoke developmental defects at late stages of gametogenesis, while genes that do so at earlier and meiotic stages are rare. The gametophytic sterility due to defects in late gametogenesis has a lesser effect on seed fertility than the sporophytic sterility due to premeiotic and meiotic defects.
It is unclear which components of the mechanism lead to such bias, but it is known that the strength of reproductive barriers is proportional to the genetic distance between two species Coyne and Orr , , Moyle et al. Actually, there are no cases of F 1 hybrid inviability in intraspecific crosses of O. Thus, the reproductive isolation is incomplete between indica and japonica. Hybrid breakdown is defined as sterility or weakness observed in the F 2 or later hybrid generations while the F 1 hybrids grow normally with good fertility.
In general, fewer case studies of hybrid breakdown than of F 1 hybrid incompatibility have been published and therefore the molecular basis of hybrid breakdown remains obscure. The genetics of hybrid breakdown have been studied in rice Fukuoka et al. Examples are the gene pairs hwe1 and hwe2 h ybrid w eakness- e -1 and - e -2 Kubo and Yoshimura , see also Fig.
The double recessive homozygote for hwe1 and hwe2 causes poor vegetative growth and complete sterility, but the molecular basis has not yet been elucidated. On the other hand, hbd2 and hbd3 were found to encode casein kinase I and NBS-LRR, respectively, and the hybrid breakdown was attributed to an autoimmune response Yamamoto et al.
Similarly, F 1 hybrid necrosis in Arabidopsis, tomato, and lettuce, was found to be due to epistatic interactions between pathogen resistance genes Alcazar et al.
These findings indicated a link between immune response systems and postzygotic RI development in plant evolution. The three genes, hsa1 , hsa2 and hsa3 h ybrid s terility- a - 1 , - 2 and - 3 , which are located on rice chromosomes 12, 8 and 9, respectively Fig. The recessive gene hsa1 causes sporophytic sterility and sterility segregates at a 3: 1 ratio in selfed progeny of the hsa1 heterozygotes.
On the other hand, hsa2 and hsa3 cause gametophytic sterility sterility phenotype determined by gamete genotype resulting in segregation distortion nearly equal to a 0. Because the hsa1 gene is recessive, interaction of these genes has no significant effects on F 1 hybrid phenotypes, which is why this sterility phenotype is a case of hybrid breakdown.
Together with epistasis-based allelic interactions, a variety of other epistatic interactions seem to contribute to postzygotic RI. Many RI genes, which were found in genome-wide surveys including QTL analysis and CSSL analysis, have been detected in a variety of cross combinations between different rice cultivars and species. In contrast, through all my previous studies Kubo and Yoshimura , , Kubo and Yoshimura , Kubo et al.
More recently, my data is suggesting that several genes relating to this genetic network still remain to be identified. Because all these genes were identified in an intraspecific cross, an equal number or more genes should be expected to be involved in postzygotic RI of crosses between more remotely related parents.
However, there are no reports of similar gene numbers in other cross combinations, suggesting that we have identified only a very small fraction of the genes involved in plant postzygotic RI. It is intriguing that such a large number of RI genes have developed at subspecies level and how they may have contributed to rice speciation. Epistasis has become a central genetic concept in understanding postzygotic RI as well as other quantitative traits.
Despite this importance, epistasis has been elusive. Among several types of epistasis, digenic interaction has often been observed as digenic segregation patterns like 1 or 5 Fukuoka et al. However, there are few studies that have characterized multiple-gene interactions with more than two unlinked loci.
Furthermore, we have never established exactly how many genes were involved in individual incompatible phenotypes. The reason is that dissecting complex genetic networks requires hard work and a lot of time. How can such networks be untangled? To date, CSSL have proven to be a powerful tool for the positional cloning of genes, and the evaluation of gene-gene as well as gene-environment interactions for many types of traits Doi et al.
Multiple concurrent introgressions produced by intercrossing different CSSLs provide an important source of segregating populations to evaluate multiple-gene interactions.
Additionally, reciprocal sets of CSSL series are useful for solving the complex network problem and enable us to specify the number of participant genes in a network. If a sterility phenotype is masked in a certain genetic background, we may postulate the existence of additional interacting genes Fig.
Conversely, if the same phenotype is consistently observed in two alternative genetic backgrounds, we may conclude that the genes under study represent the complete set, and no more genes may be required to control the sterility phenotype.
The effects of adaptive evolution on gene sequences, gene expression levels and the resulting molecular pathways, and how RI between divergent populations develops in this evolutionary process are questions of general biological interest. A tendency toward linkages between major morphological genes and RI genes has been observed in the analysis of series of CSSLs. For example, the replacement of a chromosome segment in the Asominori genome by the corresponding segment from the cultivar IR24 that contained the RI genes S24 and S35 , introduced IRlike morphological traits including narrow grains and increased number of grains per panicle Fig.
Additionally, S24 was very tightly linked to another hybrid female sterility locus, S31 Zhao et al. Other RI genes also tend to tightly or loosely link with major trait genes such as heading date Hd3a , Hd1 and S26 on chromosome 6, DTH8 and hsa2 on chromosome 8 Kojima et al. Among 10 RI genes mapped on rice chromosomes Fig. Traits such as heading date and biotic stress resistance probably had a significant role in rice evolution.
These gene clusters appear related to the indica-japonica differentiation and therefore should become a focus of molecular studies into rice evolution and domestication. Because M-V linkages in plants are responsible for linkage drag, their knowledge is critical to crop breeding. Chromosome maps showing gene clusters containing RI and morphological genes on the short arms of rice chromosomes 1 and 5. AIS 1 showed increased grain numbers per panicle compared to Asomiori [Asominori: AIS 34 showed reduced grain width compared to Asomiori [Asominori: 3.
For comparison, grain number and grain width of IR24 donor were GS5 on chromosome 5 also regulates grain width Li et al. Molecular genetics studies in rice have revealed that clusters of adjacent interacting genes and epistatic interactions are involved in the mechanism of F 1 hybrid sterility.
These studies suggest that the gradual accumulation of mutations of functionally related genes promoted the development of RI in the evolution of diverging populations. Consequently, the genetic network underlying RI evolution appears more complex than generally thought.
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