Sterility in mammalian hybrids is in a good agreement with Haldane’s rule that “when in the F1 offspring of a cross between two animal species or races one sex is absent, rare, or sterile, that sex is always the heterozygous sex”20. Several hypotheses have been proposed to explain the genetic basis of this rule. Among them, the dominance and “faster male” hypotheses are considered the most plausible2122232425. The dominance model ascribes the predominant inviability/sterility of the heterogametic sex to the alternative fixation of X-linked recessive mutations. The higher the ratio between recessive and dominant mutations of incompatibility, the larger the time lag between hetero- and homogametic sexes in the evolution of hybrid unfitness26. The “faster male” hypothesis suggests that male fertility alleles evolve and diverge faster due to divergent sexual selection. At the same time, strong sperm selection leads to increase of the stringency of male meiotic checkpoints2527. In mammals, male meiosis is very sensitive to genetic and chromosomal aberrations. Meiotic mutants and knockouts affect meiosis earlier and more severely in males than in females28 and this amplifies the effects of genetic and chromosomal incompatibility on the fertility of male hybrids.