Abstract

Genietically controlled distortions of the normal proportions of functiolnal gametes from heterozygotes are occasionally detected as departures from Mendelian rules. Few well-analyzed cases of this kind have been reported in animals. We have recently found a new case of distortion in the house mouse in which an elemenit acting in segregation and recombination like a mutant gene greatly reduces the probability of its own transmission through sperm, although it is transmitted normally through eggs. In this preliminary paper, we will report the results of breeding experiments that establish the above diagnosis, and the outcome of the first tests of two hypotheses concerning the mechanism by which the effect is produced. In the few cases of this kind analyzed in insects and mammals, the aberrations are also confined, as in our new case, to proportions of male gametes. In Drosophila pseudoobscura, males with a mutation known as sex-ratio in the X chromosome produce chiefly daughters since the mutation causes the Y chromosome to be lost in spermatogenesis so that chiefly X-bearing sperm are formed. ' In Drosophila melanogaster, a mutation in the second chromosome, knowit as segregation distorter (SD), causes the SD-bearing chromosome to be tralnsmitted by males to most of the offspring, up to more than 99 per cent. The exact mechanism is not known, but it appears to involve interference by SD with the production or function of normal sperm containing the homologue of the SD chromosome. 2 3 In the house mouse, a series of mutant alleles (t-alleles) in one region of the ninth linkage group has been identified; in many cases the mutant allele, usually lethal or semilethal, is transmitted by heterozygous males to a great majority (80-99%) of the offspring. The same alleles are transmitted in normal proportions by female heterozygotes.4 Certain t-alleles that are fully viable when homozygous are transmitted by heterozygous males in low ratios, as is the case with the factor to be described. The mechanism in most of these cases is not established but in one case may involve effects of the mutant allele on sperm function after meiosis.5,6 The niew factor that we have found in the mouse is referred to as Low ratio (Lr). We have been able to follow its transmission through some 9 or 10 generations because of its linkage with a dominant marker T (Brachy or short tail) in the ninth linkage group. When Lr occurs in the same chromosome with T (T Lr/+-+), it causes T to be transmitted by males to about 14 per cent of the offspring. Complete results for the first five generations are shown in Table 1. Daughters receiving T and Lr from. their father transmit T to their progeny in normal ratios (0.5). Brachy (T Lr) sons of these daughters again transmit T to about 14 per cent of their off spring (Table 1).

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