The genetic control of the sterility of male hybrids between certain laboratory and wild mice (Mus musculus L.) is investigated. The observed sterility is, by definition, hybrid sterility since both parental forms (i.e. wild and laboratory mice) are fully fertile, their male offspring displaying small testes with arrest of spermatogenesis at the stage of spermatogenesis or primary spermatocytes. Results of genetic analysis as well as the failure to detect any chromosomal rearrangements point to a genie rather than a chromosomal type of hybrid sterility.
Fifty-three wild males were classified into three sets, after mating with C57BL/10 inbred females, according to the fertility of their male progeny (set I – only sterile sons; set II – only fertile sons; set III – both fertile and sterile sons). The wild males of set I, which yield only sterile male offspring with C57BL/10 females, sire sterile sons also with females of the following inbred strains: A/Ph, BALB/c, DBA/1, and AKR/J, whereas the same wild males produce fertile offspring with females of C3H/Di, CBA/J, P/J, I/St and F/St inbred strains.
The described hybrid sterility seems to be under the control of several independently segregating genes, one of them (proposed symbol Hst-1) being localized on chromosome 17 (linkage group IX), 6 cM distally from dominant T (Brachyury). A chance to search for the mechanism of hybrid sterility is provided by the finding of two laboratory inbred strains, C57BL/10 and C3H/Di, differing with respect to the Hybrid sterility genetic system only at the Hst-1 gene.
Hst-1 is closely linked but apparently not identical with the sterility factor of recessive t alleles of the T locus.
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