Asymmetry and polymorphism of hybrid male sterility

X–Y Interactions Underlie Sperm Head Abnormality in Hybrid Male House Mice

First, the specificity of X—Y incompatibilities to sperm abnormality delimits the search for candidate loci to a specific spermatogenic time point and cell type, thereby reducing the genetic complexity of hybrid male sterility. Are there any cases of variation within species for traits seen in the hybrids?

In what way do F1 males of reciprocal interspecific crosses differ from one another? During this final stage of spermatogenesis, chromatin is progressively remodeled and condensed, and nuclear morphology undergoes a dramatic transformation, culminating in the highly differentiated structure of mature spermatozoa reviewed in Oliva and Castillo The superscripts denote particular strains within species.

The genetic architecture of X—autosome incompatibilities in F1 males This and previous studies demonstrate that X—autosome incompatibilities are essential for sterility and subfertility in F1 hybrid male house mice. Dark boxes show chromosomes from M. X overexpression persists in postmeiotic round spermatids, and the negative correlation between whole testis X expression and reproductive parameters is strongest for sperm morphology.

Are interspecific F1 hybrid males usually larger or smaller than the pure species males? Suppose an allele on the X chromosome from M. Thus, the effect of X—Y incompatibilities on sperm morphology may explain the complete absence of M.

Thus, candidate gene-targeted fine-scale mapping on the X could accelerate identification of the X-linked component of this X—Y incompatibility.

Asymmetry and polymorphism of hybrid male sterility during the early stages of speciation in house mice. Thus, the X—autosome incompatibilities that underlie disrupted MSCI may be a major cause of the severe sterility phenotypes that, in this study, were unique to the F1 generation.

These results provide insight into the genetic architecture of F1 male sterility, and help to explain genome-wide patterns of introgression across the hybrid zone. The genetic architecture of sperm abnormality in hybrid males We previously suggested that incompatibilities between the M.

We recently discovered that widespread overexpression of the musculusPWK X chromosome on an F1 autosomal background is explained by partial failure of meiotic sex chromosome inactivation MSCI in primary spermatocytes Good et al. This suggests that even moderate levels of sperm abnormality could have large negative effects on male fitness in natural populations.

In mice, sperm head morphology is highly correlated with competitive ability Immler et al. Which of the following hybrids would be most affected by this deleterious genetic interaction: Incomplete chromatin compaction is a common cause of abnormal sperm head morphology in mammals Balhorn ; Revay et al.

In the cross between females of M. All other things being equal, which sex would expect to be more adversely affected in interspecific F1 hybrid crosses? Second, although excess sperm abnormality does not reduce the fecundity of M.

Refer to Table 1 above.

Exercise 1

We did not, therefore, expect the musculusDOM X-9 introgression to rescue sperm phenotypes. However, we would still expect a more gradual recovery in these phenotypes as deleterious M.

Finally, suppose that the deleterious effect of the X chromosome allele is recessive and that the Y chromosome lacks the X-linked loci.

In contrast, if simple incompatibilities between the X and one or two autosomal loci are sufficient for F1. These two species still interbreed in nature and form a hybrid zone in Europe; because the hybrid males are mostly sterile, gene flow between the species is impeded.

In birds, sex determination is the reverse of that in mammals: We dissected the relative contributions of X—Y and X—autosomal dominant incompatibilities to three reproductive phenotypes in an generation backcross experiment in which the M. Thus, the genetic architecture of this sterility phenotype is distinct from that underlying reduced testis weight and sperm count.

When hybrids between species are partially or completely sterile or inviable, the cause of that sterility or inviability is usually improper interactions of alleles at different loci. RTW is the mean testis weight in mg divided by the body weight in gand RSVW is the mean seminal vesicle weight in mg divided by the body weight in g.

What is the genetic composition of the X chromosome of those same males? Similar in appearance, M. While autosomal genes play the major roles in chromatin repackaging and condensation e.

We found a significant negative effect of X—Y interactions that was specific to sperm morphology:Critical Review: Asymmetry and Polymorphism of Hybrid Male Sterility During the Early Stages of Speciation in House Mice.

In this study, the researchers sought to determine the genetic cause of male sterility in house mice when there was interbreeding among different but related species. sterility often appears earlier in species divergence than hybrid inviability [7,8]; and third, heterogametic isolation generally appears earlier in.

Regardless, the observation of polymorphism at multiple loci that have a large impact on F 1 hybrid fertility suggests that resolving the overall genetic architecture of hybrid male sterility may require considerable population-level sampling within both M. musculus and M.

domesticus (Vyskocilová et al. ). The unexpected combination of genetic. Request PDF on ResearchGate | Asymmetry and Polymorphism of Hybrid Male Sterility During the Early Stages of Speciation in House Mice | House mice offer a powerful system for dissecting the genetic basis of phenotypes that isolate species in.

If hybrid male sterility is the product of multiple incompatibilities that act at different time points in spermatogenesis, then a smaller number of interactions might underlie any one sterility phenotype. found significantly smaller testes and fewer sperm in hybrid male progeny of most crosses.

Second, in some crosses hybrid male sterility was asymmetric and depended on the species origin of the X chromosome.

Asymmetry and polymorphism of hybrid male sterility
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