Genetic studies on male sterility of hybrids between laboratory and wild mice (Mus musculusL.)

Abstract

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. 13-2

Chromosomal and genic mechanisms of reproductive isolation: the case of Suncus murinus

“…The system of hybrid sterility, which was found in the S. murinus, appears to be somewhat similar to that discovered by Forejt and Ivanyi (1977) (Forejt and Ivanyi 1977). Several other monogene systems of hybrid sterility have been found in the house mouse (Forejt 1996).…”

Genetic Dissection of a Key Reproductive Barrier Between Nascent Species of House Mice

“…We quantified five diagnostic measures of subfertility and sterility in house mice: testis weight (Iványi et al 1969;Forejt and Iványi 1974), sperm density (Searle and Beechey 1974;Storchová et al 2004;Vyskočilová et al 2005), sperm head morphology (Oka et al 2004;Storchová et al 2004;Kawai et al 2006), proportion of abnormal sperm (Kawai et al 2006), and cross-sectional area of seminiferous tubules. Although we did not perform additional matings to directly examine the fertility of each F 2 male, the measured phenotypes allowed a fine-scale dissection of different components of hybrid sterility.…”

“…In addition, M. m. musculus and M. m. domesticus exhibit prezygotic isolation, including preferences for mates from the same subspecies (Laukaitis et al 1997;Talley et al 2001;Ganem 2002, 2005;Smadja et al 2004;Ganem et al 2008) and higher fertilization rates by sperm from the same subspecies when females are multiply mated (Dean and Nachman 2009). The most direct evidence for reproductive isolation comes from laboratory crosses involving wild-derived inbred strains, where F 1 hybrid male sterility is routinely observed, usually without hybrid female sterility (Iványi et al 1969;Forejt and Iványi 1974;Storchová et al 2004;BrittonDavidian et al 2005;Vyskočilová et al 2005Vyskočilová et al , 2009Good et al 2008a,b).…”

“…The only gene known to cause hybrid sterility in vertebrates, Prdm9, resides on chromosome 17 in house mice (Forejt and Iványi 1974;Forejt 1996;Mihola et al 2009). Consistent with a Dobzhansky-Muller incompatibility framework, the sterility effect of Prdm9 requires interaction with additional, unidentified loci (Forejt and Iványi 1974;Forejt 1996;Mihola et al 2009).…”

“…The only gene known to cause hybrid sterility in vertebrates, Prdm9, resides on chromosome 17 in house mice (Forejt and Iványi 1974;Forejt 1996;Mihola et al 2009). Consistent with a Dobzhansky-Muller incompatibility framework, the sterility effect of Prdm9 requires interaction with additional, unidentified loci (Forejt and Iványi 1974;Forejt 1996;Mihola et al 2009). Backcrosses between M. m. domesticus and Mus musculus molossinus (a hybrid between M. m. musculus and Mus musculus castaneus) have identified several autosomal QTL that affect hybrid sterility when the entire M. m. molossinus X chromosome is present on the M. m. domesticus genetic background (Oka et al 2007).…”