Hybrid incompatibility is a term to describe the observed facts that mating between close species produce inviable or sterile offsprings that have low fitness. These phenomena show in a wide range of organisms including plants, animals and even microorganisms. Incompatibility shown in interspecific hybrid is believed as the main cause of post mating reproductive isolation which is in term a hallmark of speciation. Those sterility and lethality are usually resulted from improper genetic interactions that diverging species in one of the hybridizing lineages. This paper is aim at studying genetic of hybrid incompatibility in different perspectives by finding the different causes of hybrid incompatibility such as the evolutionary causes of divergence, the mode of development of hybrid incompatibility and how the degree of incompatibility takes effect on the hybrid fitness.
Interspecific hybrid incompatibility is important in species diversification and species maintenance which are key topics in evolutionary biology. Speciation involves a series of step which multiple reproductive barrier accumulate over time progressively from hybridization producing viable offspring, followed by hybrid infertility and inviability and finally complete pre-zygotic reproductive isolation. Consequently, Sight on the genetic basis of hybrid incompatibility is of great interest for understanding the evolutionary process of speciation. Previous research found that the causes leading to this post-zygotic reproduction barriers can be at different level. For example, epigenetically, the chromatin binding proteins may not be able to interact with chromosomes from another species in a hybrid, making gene transcription misregulated; at chromosomal level that change in ploidy number which usually occurs in plants hybrid or difference in chromosome number such as hybrid of horses and donkeys; at molecular level that negative epistatic interaction of alleles at different genetic loci.
Mode of hybrid incompatibility
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Though interspecific hybrid incompatibility being a reproduction barrier is a great driving force to speciation, it faces a serious problem that how such a maladaptive inviability and infertility could evolve by natural selection. One of the theories trying to explain how incompatibilities between closely related species develop without either of the them going through an adaptive valley is the Dobzhansky-Muller Model. It posits that hybrid incompatibility is unlikely to be arisen from only a single change at one locus due to underdominance (viable AA or aa but inviable Aa) that such hybrid being heterozygotes have lower fitness should an allelic substitution not take place by natural selection. Even if genetic drift exist, the population need to be persisting at a very low population size so the possibility is relatively low. In contrast, Dobzhansky-Muller incompatibilities result from negative epistatic interaction between alleles located at least at two loci.Those incompatibility casuing gene, called 'complementary gene' show no deleterious effects within either population but dysfunction with genes from other species when brought in hybrid. (Fig.1)
The basic model is that two allopatric populations starting with common ancestral genetic background, while accumulation of genetic change continues along their divergence such that allele substitution at different loci occur in the separated populations. The derived alleles are neutral or even beneficial in their own genetic background but incompatible with the later derived allele at different loci in another population. When considering many loci, the accumulation of complementary gen can be shown by the following diagram:
The two lines that forming a V shape represent the two lineage from a common ancestor and both population have all their allele lowercase fixed at initial. Time proceed upward and the first allele substitution takes place at locus a, then locus b followed by locus c and so on. The arrows show possible incompatibilities due to epistatic interaction between loci form the two populations. Some principle can be concluded from the figure. Firstly, according to the graph, since the arrows never point upwards, it indicate incompatibility must occur between two loci that both have allele substitution, which in term alleles at undiverged loci must be compatible with those diverged loci as the two population share the common genetic background. Secondly, later substitutions are more potent in causing incompatibilities than that of the earlier (D may be incompatible with c,B,a but B could only be incompatible with A)which suggest the rate of increase of intensity of reproductive isolation may be faster than first order (Snowball effect). Thirdly, all the incompatibilities are initially asymmetric that for example C could be incompatible with a but b cannot. This further deduce that a evolutionarily derived allele(uppercase) tend to be involved in incompatibility more than a ancestral allele(lowercase).The reason is that when considering all the possible types of incompatibility, there are derived allele-derived allele and derived allele-ancestral allele interaction but not including a ancestral allele-ancestral allele type.
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Other than Dobzhansky-Muller Model, there are another principle concerning hybrid gender-the Haldane's Rule. It states that when one sex in the interspecific hybrid is missing, sterile or rare,that sex is heterozygous sex. Haldane's Rules suggest different hypothesis that heterogametic sex usually have lower fitness than homogametic sex. The most popular one is the dominance hypothesis, suggesting a genetic theory similar to the sex-linked defects in human such as colorblindness and haemophilia. It proposes that the dominance of incompatibility allele play a role in the hybrid fitness and evidence was found to prove they are on average partially recessive. The hybrid of heterogametic sex carrying only a single sex-linked gene will suffer from the negative effect of the alleles no matter of the dominance. However, a homogametic sex hybrid will suffer only if the incompatibility allele is dominant because a recessive allele will be covered by another allele in the second X-chromosome. As a result, defects is more visible in heterogametic sex hybrid than homogametic one. Second, research data support a faster-X theory that genes on X-chromosome evolved much faster than that on autosome which in term a greater effect on hybrid incompatibility. In fact, there are many life example such as inviable male hybrid of Drosophila and significant deficiency of males mules at birth confirming the general truth of Haldane's Law.
Hybrid incompatibility in plants:
Spontaneous hybrid was used to be recognized as an important driving force of speciation as there are apparent evidence suggesting the case many plant species have hybrid ancestry. New species can be arisen by hybridization much more easier in plant since the hybrid plants can still reproduce even it is sterile by different mechanism of asexual reproduction such as vegetative propagation. However, a recent research found that the occurrence of spontaneous hybridization is not as ubiquitous as frequently believed. Instead, the occurrence of spontaneous hybridization is partially restricted to part of families and an even smaller proportion of genera. In plant, the deleterious phenotype of hybrid is often due to an autoimmune syndrome called hybrid necrosis. There are several mechanisms underlying hybrid necrosis but apparently often involve the immune system. One example of hybrid necrosis is tapetal-specific that causing male sterility which usually found in hermaphroditic plants. It was found that the cytonuclear incompatibility plays a major role in this developmental aberration. A male-sterile phenotype is observed in the hybrid with tapetal deterioration, which tapetal tissue nurtures pollen mother cells. Mitochondrial genes triggers a standard pathway of programmed cell death(PCD) which destroy the tapetum, while nuclear genes suppress the male sterility and restore pollen fertility by a counteracting measure. There are different mitochondrial genotypes triggering cell death in different ways by altering the complex regulatory cascade leading to PCD, while each of them have a specific set of matching nuclear genes that block PCD and restore normal function. As a result, the tapetal development is regulated by the balance of disruptive effects of mitochondria and the defensive effect of the nuclear genes. However, this delicate mitochondrial-nuclear balance is disturbed in hybrid and thus upset the regulatory control of programmed cell death, causing tapetal abnormalities and male sterility. Moreover, Sometimes PCD further affect tissues throughout the plant as PCD is involved in part of the development of tissues like leave and xylem. Also, PCD is a defensive mechanism against pathogen in plant cells which imply that misregulation of PCD can lead to serious problem of cell death. This types of cytonuclear incompatibility may contribute to the investigation of evolution as rapid evolution of the mitochondrial and nuclear genes is expected. Hybrids from crosses between Nemophila menzesii and a diverged population show symptoms such as stunted growth, thickened and curled leaves, aberrant petals and anthers with little or no pollen, which match the characteristics of the PCD-induced aberrations.
Another case of hybrid necrosis was discovered when studying the specie Arabidopsis thaliana. Cross between A. thaliana strains show hybrid necrosis which was found to be a Dobzhansky-Muller-Type Incompatibility Syndrome, involving a negative epistatic interaction between 2 to 4 loci. A highly polymorphic NB-LRR genes, which is most common resistant gene in plant was mapped and found responsible for the improper regulation of immune system in hybrid. The NB-LRR expression is normally regulated by a trans-acting element encoded at second loci which a failure of coevolution of the two interacting loci may disturb the balance of the interaction, leading to ectopic activation. Hybrid show lower threshold for activation of active immune response and some hybrid may have enhanced resistance against pathogen when comparing to their parents. Typically, mitochondrial genes are matrilineally transmitted only through seeds but not through pollen while nuclear gene are biparentally transmitted. In this case, hybrid survival is not dependent on the direction of the cross, that in other words which species act as the maternal parent, demonstrating it is not caused by aberrant nuclear-cytoplasmic interactions like those involved in cytoplasmic male sterility. This type of hybrid necrosis is experimentally found temperature sensitive which hybrid suffer from lethality at its typical habitat temperature but the autoimmune response is greatly suppressed at a higher temperature. The temperature-dependent effect suggests a quantitative incompatibility which the deleterious phenotype is subjected to the dosage of the incompatible alleles.
Hybrid incompatibility in animals:
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Although a clear illustration regarding the hybrid sterility and inviability remains black boxes, a few hybrid incompatibility genes were identified with the powerful innovative genetic tools being invented such as lost of function muataion, chromosomal duplications and deletions and DNA engineering. A 'Dobzhansky-Muller" type incompatibility was identified in a platyfish species. Hybrid between platyfish Xiphophorus maculatus and a related species the swordtail Xiphophorus helleri show inviability. Also, backcross hybrid of those species often develop malignant tumor and eventually die. With the help of molecular genetic analysis, a X-linked hybrid incompatibility gene Xmrk-2 which code for a novel receptor tyrosine kinase was found misexpressed in hybrid, leading to cancer formation. Xmrk-2 gene functions as a spot producing gene in platyfish with a repressor gene locating at an autosome. The autosomal repressor is missing in hybrid resulting in improper regulation of the Xmrk2 gene expression. More HI genes were discovered during studies on a frequently used genetic tool -Drosophila. Those identified incompatibility genes include Odysseus-Homeobox (OdsH), Lethal hybrid rescue (Lhr), Hybrid male rescue(Hmr) and Nup96 genes. Ods cause male sterility in hybrid cross between D. simulans and D. mauritiana as it encodes a duplicated transcription factor which is misregulated in the testes of the hybrid.Research found loss of function mutation of Hmr gene in D. melanogaster and Lhr in D. simulans suppress hybrid male lethality. Both gene demonstrate asymmetry in causing hybrid lethality which is stated in Dobzhansky-Muller model by the result that deletion mutation of those alleles of another species cannot rescue the hybrid. Among those incompatibility genes, Nup96 seem to be more informative in nowadays study. Nup96 gene codes for a protein that stably bound to the nuclear pore complex which is the largest macromolecular complex in eukaryotes. The Nup96 nucleoporins play a structural roles in nuclear pore compex mediating nucleocytoplasmic trafficking of RNAs and proteins. In hybrid cross between D. melanogaster and D. simulans,a D. simulans, Nup96 allele cause lethality in hemizygous for the D. melanogaster X chromosome but not in hemizygous for the D. simulans X chromosome. The observation match the Dobzhansky-Muller model predication that a D. simulans allele of Nup96 would not be incompatible with loci on its own X chromosome.Nup96 protein is found interacting with others nucleoporins such as Nup75, Nup107, Nup133, Nup160, Seh1, Nup37, and Nup43 to form a Nup 107 subcomplex. Sequencing analyses of polymorphism of those genes suggest a trend of adaptive coevolution between Nup96 and some of its interacting proteins. Such coevolution event may provide a new model different from the assumption of population genetic that substitution take place independently. Comparing with independent substitutions model, non-independent evolution may speed up divergence of hybrid incompatibilities since substitutions at 1-locus increase the probability of substitutions at interacting loci within a lineage. Also, Coevolution of interacting genes may concentrate substitutions in one lineage which imply a increase in possibility of derived-ancestral allele hybrid incompatibilities, opposing to the predication of Dobzhansky-Muller Model.
Effect of incompatibility on fertility and viability:
A past experiment investigated whether hybrid incompatibility affect sterility and lethality differently using two yeast species S. cerevisiae and S. paradoxs. Fertility and viability of the yeast were measured by the sporulation frequency and the clonal growth rate respectively . The heterozygous F1 hybrids were not used in the test as recessive incompatibility may be masked. Instead, homozygous F2 hybrids formed by autodiploidization of the F1 gamete were examined. Result show that for each F2 individual, the growth-based was much higher than sporulation-based fitness, indicating hybrid sterility is more pronounced than hybrid viability. A possible molecular mechanisms is that a S. cerevisiae nuclear gene MRS1 was found incompatible with a S. paradoxs mitochondrial gene COX1. This cytonuclear incompatibility disturbs cellular metabolism on non-fermentable medium where yeast sporulates and therefore cause hybrid sterility. Moreover, meiosis-related genes was found fast evolving in the yeast which is a possible explanation for the observation that fertility-related incompatibilities are more common than viability-related incompatibilities.
Interspecific hybrid incompatibility is one of the causes of reproductive isolation between species which is a defining feature of the biological concept of species. Knowing the genetic basis of hybrid incompatibility is therefore a crucial procedure of discovering the origin of speciation. As genetic drift and selection continues after speciation, the split species continue to diverge and the intensity of incompatibility will only keep on increasing. Therefore, finding a incompatibility gene not necessarily mean finding a speciation gene. As a result, speciation genes should be defined as evolved to cause incompatibility only at the time of speciation but it poses a great difficulty to isolate a speciation gene after speciation have taken place over millions years. However, hints about the phylogenetic relation among species may be obtained by observing the incompatibility pattern of hybrid crossed from different related species. For example, a Nup96-dependent lethality show in hybrid between D. melanogaster-D. simulans and D. melanogaster -D. sechellia, but not in D. melanogaster- D. mauritiana hybrid suggesting D. mauritiana may have speciated before D. simulans and D. sechellia. Apart from this, more evolutionary event could be predicted with the incidents that all non-synonymous substitution of Nup96 allele of D. simulans are also found in D. mauritiana ,which indicate Nup96 allele may had diverged prior to the divergence of D. simulans and D. mauritiana. Also, a gene locating on X chromosome incompatible with Nup96 alleles to cause lethality should have diverged on the D. melanogaster lineage due to the occurrence of lethality only on hybrids with the D. melanogaster X chromosome, neither with D. simulans nor D. sechellia .
Evolutionary forces that drive the divergence of speciation genes
Additional to the identity and the characteristic of the speciation genes, biologists are also interested in understanding the driving force to the divergence of speciation genes. Increasing evidence show that hybrid incompatibility gene evolves as a by-product of adaptive evolution and is rapidly evolving. For example, by gene mapping and DNA sequencing, Nup96 gene was found diverged among Drosophila species with significant excessive non-synonymous substitution relative to synonymous substitution, demonstrating Nup96 allele is under positive natural selection rather than genetic drift. In addition, new hypotheses propose intragenomic conflict may take a part in which meiotic drive may contribute to the evolution of postmating reproductive isolation. Past research suggested that independent segregation of mendelian principle may not be as universal as believed but in fact the non-mendelian segregation is masked in population because suppressor mutation quickly fixed after a distorter arises. A autosomal repressor allele of sex-ratio distortion was found to associate with hybrid sterility in
To understand speciation, first we should know the origin of reproductive isolation. Although the majority of the truth of hybrid incompatibility remains uncertain, it provides a insight for us to investigate the evolutionary divergence among species. With the efforts of scientists and innovation of new technology, a more realistic and detailed model about genetic of hybrid incompatibility can be constructed and finally bring us closer to the process of the speciation.