The three major regions (T, tail-determining; A, abnormal transmission ration; L, embryonic lethality) of the t complex on the murine seventeenth chromosome can interact to influence male reproduction (Lyon & Mason, 1977; Hammerberg, 1981). Evidence is presented here that suggests: (1) the presence of a polymorphic system within the T region that influences quasi-sterility in the male; (2) the existence of enhancing factors of transmission ratio distortion; and (3) that preferential interactions between t-haplotypes are found to occur both cis and trans which influence transmission ratio distortion.

A computer model of a two-locus genetic system with epistatic selection was used to investigate factors influencing the probability of the origin of reproductive isolation, due to a genetic revolution following a founder event (Mayr, 1954; Carson, 1975). Restricted population size can sometimes cause such a system to drift from one equilibrium to another, which can result in loss of fitness to hybrids with the ancestral population. The chance of such an event was found to be low unless the bottleneck in population size associated with the founder event was preceded by many generations of relaxed selection. It is highest when the bottleneck is not prolonged and when the population size during the bottleneck is not too small. It seems to be difficult to achieve a high degree of reproductive isolation in one step by this method, and it is concluded that it is unlikely to be a major cause of rapid speciation, although it could be a contributory factor.

Selection for increased and for decreased expression of the sex-linked gene brindled (Mobr) in heterozygous females produced two lines with non-random X chromosome inactivation. In the High line the X chromosome marked by brindled was active in about 60% of cells, while in the Low line it was active in about 25% of cells. The whole of the difference was caused by the chromosomes carrying brindled: neither the unmarked X chromosome nor the autosomes were differentiated. There was a positive correlation between the expression of brindled in daughters and mothers. This was probably not caused by residual genetic variation, but was more probably a maternal effect similar to that described by Cattanach & Papworth (1981). On this assumption the daughters' scores were adjusted to a standard maternal score. Enzyme assays on females doubly heterozygous for brindled and for the sex-linked Pgk-1 locus proved that the percentage of brindled in the coat provided an accurate measure of the X-inactivation proportions in the blood, liver and kidney. The accuracy was improved by adjustment for maternal score. In the selection lines, brindled was always inherited from the mother. When brindled was transmitted by male parents the probability of activation of its chromosome was increased by 8 percentage points in the High line and 18 in the Low line. This effect of the parental source is much greater than has previously been reported. The responses to selection can be interpreted in terms of the Xce locus controlling the activation probability, different alleles on the chromosomes carrying brindled being selected in the two lines. If this interpretation is correct, the alleles on one or both of the chromosomes carrying brindled were different from any of the three known alleles. The different effects of male transmission in the two lines can be described as a difference between the two chromosomes in their reactions to imprinting. This difference might possibly also be due to the Xce locus.

Plasmodial formation in the Myxomycete Physarum polycephalum is under heterothallic control by a mating type (mt) locus. In natural isolates only amoebae with different mt alleles are able to cross to form diploid plasmodia. A class of mutants isolated from heterothallic amoebae, together with the variant strain CL, is able to form plasmodia in pure clones, designated as selfing. Non-selfing mutants have been isolated from CL and from other selfing amoebae.

This paper reports the isolation and analysis of 64 non-selfing derivatives (designated Npf−) from seven selfing (Het−) strains. The Npf− mutants could be grouped into eight classes on the basis of their crossing and complementation patterns. The possible significance of these mutants is discussed.

Spleens with black pigment in them were found in 4–57% of mice from 17 stocks, all sublines of C57BL or with significant C57BL ancestry. Splenic lipofuscinosis was absent from 16 stocks, including three C57BL/6By × BALB/cBy recombinant - inbred lines. Progeny testing showed all C57BL/6J mice to be equally likely to develop black spleens. The penetrance of lipofuscinosis differed between sublines but not between the sexes or between laboratories. Susceptibility to lipofuscinosis showed dominant, autosomal, inheritance in F1 hybrids. Observations on backcrosses and on recombinant inbred lines and their intercrosses indicated the existence of two genetic factors. Splenic lipofuscinosis was prevented either by a deficiency of melanin or by homozygosity for a non-C57BL allele close to the c-p region of chromosome 7. The presence of a C57BL allele at a locus on another chromosome is necessary for lipofuscinosis to occur.

The isolation of a temperature sensitive pts I mutant which fails to utilize lactose provides strong evidence that Klebsiella strain CT-1 utilizes lactose via a phosphoenolpyruvate dependent lactose-phosphotransferase system (PTS-lac). We designate this lactose utilization system elu for evolved lactose utilization. Analysis of a series of Lac− mutants identifies two genes, eluA and eluB, whose function is required for lactose utilization by this pathway. The functions specified by these genes are not known, but neither locus specifies the hydrolytic enzyme phospho-β-galactosidase. A mutant of CT-1, strain RPD-2, exhibits a half-maximal growth rate at a lactose concentration 40 fold lower than that of strain CT-1; and it has a Km for lactose uptake that is 40 fold lower than that of strain CT-1. That mutation defines the locus eluC, which is assumed to specify the enzyme Il(lac) of the PTS-lactose system. From the observations that (i) cellobiose induces the phospho-β-galactosidase enzyme, (ii) pregrowth in cellobiose dramatically reduces the growth lag when cells are shifted into lactose minimal medium, (iii) eluB mutants exhibit a growth lag when shifted into cellobiose minimal medium, and (iv) lactose induces a phospho-β-glucosidase enzyme; we speculate that the phospho-β-glucosidase enzyme is the same enzyme as the phospho-β-glucosidase that normally functions in cellobiose metabolism. We conclude that the original mutation that allowed CT-1 to utilize lactose was a regulatory mutation that permitted inducible expression of the eluC gene.

Introducing a new genetic model called the discrete allelic-state model, the evolutionary change of genetic variation of quantitative characters within and between populations is studied under the assumption of no selection. This model allows us to study the effects of mutation and random genetic drift in detail. It is shown that when the allelic effects on phenotype are additive, the rate of approach of the genetic variance within populations to the equilibrium value depends only on the effective population size. It is also shown that the distribution of genotypic value often deviates from normality particularly when the effective population size and the number of loci concerned are small. On the other hand, the interpopulational variance increases linearly with time, if the intrapopu-lational variance remains constant. Therefore, the ratio of interpopulational variance to intrapopulational variance can be used for testing the hypothesis of neutral evolution of quantitative characters.

A mutation to an apparently new allele at the W-locus of the mouse arose spontaneously in a cross between two inbred strains. Heterozygotes have a broad white sash, leading to the name and symbol sash, Wsh. Homozygotes are black-eyed whites which are viable, fertile and not anaemic, although the gene does cause mild haematopoietic defects. The original mutant animal also carried a spontaneous recessive lethal mutation on chromosome 5, mapping at 2 cM distal to the W-locus.