Do histocompatibility genes influence sex ratio (% males)?

Abstract

Breeding records for 15 of the 42 C57BL/10SnJ Congenic Histocompatibility Mouse Strains from the Special Mouse Stocks Resource (SMSR) showed three with a significant excess of male offspring. Strain B10.R111(71NS), hereafter R, gave the highest proportion of males (55.68 +/- 0.59% of 7129 newborn) which is significantly more than the proportion of male offspring (49.81 +/- 0.94% of 2853 newborn) from the C57BL/10SnJ progenitor strain, hereafter B. All mice in the SMSR colonies were fed Old Guildford 96 and Old Guildford 96W liberally on alternate weeks. Breeding females of B and R strains were established in a research colony at the Jackson Laboratory under conditions similar to those in SMSR except that they were fed Wayne Sterilizable Rodent Blox. More than 5000 inbred, hybrid and backcross fetuses were examined but no evidence of an excess of males was found. Also, there were no strain differences in the neonatal data. However, the sex ratio of the 4396 neonates was just significantly higher (P less than 0.05) than that of the fetuses, indicating some perinatal loss of females. An even greater loss of females was most probably the cause of the high sex ratios in the preliminary and follow-up surveys of SMSR R mice, which we ascribe to an interaction between the H-2 haplotype of the R strain, or a gene linked thereto, and the Old Guildford diet that is unfavourable to female survival. The sex ratio of fetuses agreed so closely with the Mendelian expectation as to indicate that the primary sex ratio was 50% males and that the R strain is not a model for the human male bias. There were no hermaphrodites or twins and the sex ratio of the fetuses in litters without resorptions was normal. These findings emphasize the variability of presumptive secondary sex ratios.