Referring to interspecific hybrids, I have the following two questions:-

Quoting from wikipedia:-

The offspring of an interspecific cross are very often sterile; thus, hybrid sterility prevents the movement of genes from one species to the other, keeping both species distinct. Sterility is often attributed to the different number of chromosomes the two species have, for example donkeys have 62 chromosomes, while horses have 64 chromosomes, and mules and hinnies have 63 chromosomes. Mules, hinnies, and other normally sterile interspecific hybrids cannot produce viable gametes, because differences in chromosome structure prevent appropriate pairing and segregation during meiosis, meiosis is disrupted, and viable sperm and eggs are not formed. However, fertility in female mules has been reported with a donkey as the father.

1) The sterility of hybrids prevents interspecific gene exchange and is necessary in case the hybrid has odd number of total chromosomes (the hybridized species has odd and even pairs of chromosomes individually), where equal meiotic division would not be possible, and is also necessary to avoid sex determination problems that may arise from such hybridizations genetically. What is the molecular (genetic) reason behind the sterility? In other words, why is the expression of primary sexual organs and its further proliferation to effect reproduction not possible, although the genes required for it are already present in the hybrids? Is this due to epigenetic mechanisms or is the reason inherent in the hybrid nature of the genome?

2) This might probably sound a bit naive, but why are these hybrids viable? They have 2 non-homologous haploid pairs of chromosomes which have a huge variety(compared to two homologous pairs) of different non-allelic genes. Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes?

Probably related to the question is the fact that certain allopolyploids are viable and become an entirely new species, but others are not. Is it because here are 2 sets of each combining species' chromosomes (and hence allowing proper meiotic pairing) or is there some other reason pertaining to the nature of the combined sets of chromosome?

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    $\begingroup$ mitosis is not affected because there is no pairing of homologous chromosomes. Meiosis is possible affected because pairing is compromised. However, non-meiotic recombinations are possible. Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes? Hybrids are not possible between totally unrelated species. The similarity of the genes and the genetic networks perhaps allows the cells to carry out normal functions. $\endgroup$
    Commented Oct 28, 2013 at 8:10
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    $\begingroup$ Can you add a referece to support your first point? Hybrid introgression and hybrids with lowered fitness (i.e. not fully sterile) has been shown to be relatively common in natural populations. $\endgroup$ Commented Oct 28, 2013 at 14:44
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    $\begingroup$ @fileunderwater Please see the edit in my question. $\endgroup$ Commented Oct 28, 2013 at 15:11
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    $\begingroup$ i think it is not just about odd number of chromosomes. Pairing would be compromised if there are no homologous syntenic regions. $\endgroup$
    Commented Oct 28, 2013 at 17:04
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    $\begingroup$ Mallett 2008 might be of interest to you. It doesn't answer the questions about genetic mechanisms, but is a good perspective on hybridization viability/sterility. $\endgroup$ Commented Dec 5, 2013 at 19:47

1 Answer 1


Davis et al. 2015 studied hybrid sterility in cats by identifying SNPs and transcriptome changes that are associated with hybrid male sterility.

They identified eight autosomal regions "involved in the function of the blood-testis barrier, gamete structural development". So it seems that the male hybrids have an altered testicular blood supply and sperm development.

More importantly, they have found a lot of altered genes on the X chromosome. It seems that a lot of regions on the x-chromosomes have duplicated. They also found "chromosome-wide upregulation of X chromosome transcripts in testes of sterile hybrids, which were enriched for genes involved in chromatin regulation of gene expression". This is a major hint that epigenetic regulation is the cause of hybrid infertility. I think this makes sense, since all (mammal) females have to shut down one x-chromosome by methylation of the x-chromosome, to prevent a doubling of gene dosage (Sex-chromosome dosage compensation). They mention that in their discussion (which is rather cryptic for my taste), too, and if I understood this correctly, males are also in need to methylate their X-chromosome (partially?). If they fail to do so, male hybrids upregulate X-chromosomal genes that in turn cause infertility. They mention a gene on the x-Chromosome called FMRP that is essential for spermatogenesis that seems to be altered in hybrids.

The focus on the x-chromosome might also answer your second question: I presume that the hybrids are viable since most genetic "damage" is concentrated on the X chromosome, while the autosomes seem to work fine. After all, autosomal damages don't carry as much weight as X-chromosomal damages, since autosomes come in pairs (in males). If one autosome has a dysfunctional gene, it is likely that his homologous partner carries the functional version. The X-Chromosome however is alone, so mechanisms like DNA-repair by homologous recombination is not possible and DNA damage can accumulate. But that is just speculation from my side (!).

They also talk about the "large X-Effect". I am no expert, but it seems that the X-chromosome is a 'hotspot for "speciation genes," that prevent genetic exchanges between closely related species' ref However I didn't understand what they were talking about, but maybe this throws your own research into the right direction.


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