The mutation load is sensitive to changes in the segregation ratio caused, for example, by biased conversion. If the distortion, measured by the force of conversion, is greater than the loss of fitness in the mutation heterozygotes, then the mutation load will be far away from its normal value. Examples are given where a small positive bias together with realistic fitness parameters increase the mutation load by more than two orders of magnitude.

In practical terms this implies that great restrictions should be placed on the use of substances and treatments that may induce mutations associated with a positive conversion bias.

(1) A tail-skin grafting method was used to test for histocompatibility differences between members of thirteen sublines of C3H inbred mice, kept in a 1 r./night gamma radiation field for twelve generations, on the average, and separated from each other by about thirty-four generations.

(2) No homograft rejections occurred, so there was no evidence to suggest that mutations at histocompatibility loci had taken place in any of these sublines. Calculations show that this finding does not conflict with the idea that a fairly large number of loci are involved, having mutation rates similar to those already known in the mouse.

The production of Inl+ recombinants was readily demonstrated in transductional crosses from Inl+ donor strains to Inl− recipient strains from different biotypes and biogroups. None of numerous crosses between different pairs of strains from biotypes 25 and 26 and the biogroup FIRN (biotypes 29, 30, 31 and 32) gave Inl+ recombinants suggesting that the inl mutation was present at the same intragenic site in all of these strains. Strains of the FIRN biogroup (Fim−Inl−Rha−Bxyl−) are thought to have descended by successive rha and fim mutations from an ancestral bacterium of biotype 25 (Fim+Inl−Rha+Bxyl−). The sites of the inl mutations in other Inl− biotypes (9, 10, 27 and 25hi) were independent and each was different from that in strains from biotypes 25, 26 and FIRN.

A haploid strain of Saccharomyces cerevisiae has been described which, on glucose medium, segregates vegetatively a high frequency of mutants with different degrees of respiratory impairment. The range of mutants seemingly encompasses both non-revertible ρ- petites and revertible point mutations resembling leaky mit- mutations. The segregants have aberrant cytochrome contents and reduced growth capabilities on fermentable sugars other than glucose; these defects apparently correlate with the degree of respiratory impairment. Genetic analysis of this mutator phenomenon has implicated a nuclear gene which appears to show specificity of interaction with the mitochondrial genome as well as a requirement for glucose repression. The mutator effect seems to extend also to the loci in mitochondrial DNA for resistance to the antibiotics erythromycin and oligomycin.

Analysis of the transposition behaviour of the P and hobo elements borne by the 31·1/CyL4 MRF (P), 23·5Δ/CyL4 MRF (hobo) and 23·5*/Cy MRF (hobo) strains in the progeny of dysgenic crosses with two ME laboratory strains (Berlin-k and dp b en bw) at 25 °C revealed that: (a) the two ME laboratory strains affect differently the transposition rates of P and hobo elements. More precisely, P element transposition is higher in heterozygotes with dp b en bw than in those with Berlin-k. In contrast, the transposition rate of hobo elements is higher in Berlin-k than in dp b cn bw heterozygotes. (b) Like P, hobo has the potential to transpose at high frequencies and to nonhomologous chromosomes, (c) The dysgenically inactive hobo elements of the 3·11 MRF strain transpose more frequently than the dysgenically active hobo elements of the 23·5 MRF strains in certain crosses, (d) There are insertion hot spots for P and hobo elements. For the P elements there are enough data to suggest that the insertion hot spots are different in the two EM strains. The data are discussed on the basis of the involvement of putative host factors in transposition regulation of the P and hobo elements.

The ftsZ gene of Escherichia coli, which codes for an essential cell division protein, is subjected to multiple regulation, as shown in part with studies using an ftsZ::lacZ operon fusion located on phage λJFLIOO. Using this same fusion, we sought to isolate regulatory mutants overexpressing ftsZ by selecting mutants able to grow on lactose. One Lac+ mutant was obtained which overexpressed the ftsZ::lacZ fusion 70-fold. The mutation responsible for the overexpression lies in a new gene, cot, located near 56 min on the E. coli genetic map. The cot mutation probably affects the transcription of a chromosomal open reading frame, 0RF1, lying downstream of the bioA gene and adjacent to the ftzZ::lacZ fusion of the λJFL100 prophage integrated at attλ. Using an ftsZ84(Ts) strain, in which there was a double selection for overexpression of both ftsZ::lacZ and ftsZ+, no Lac+Tr mutants were obtained from 3·6 × 1010 bacteria; the introduction of a mutL allele, increasing spontaneous base substitution mutation rates 75-fold, did not permit us to isolate such a mutant. We conclude that Lac+ftsZ-constitutive mutations cannot be obtained in λJFL100 lysogens by a single base substitution.

The contribution of maternal and foetal genotype to the regulation of extra-embryonic (exocoelomic and amniotic) fluid and embryonic fluid in the mouse is discussed. Three of the four inbred strains studied (A, BALB/c and CBA) had similar patterns of fluid accumulation. The fourth (C57BL) differed significantly. In the reciprocal F1 crosses between CBA and C57BL a maternal effect was present. In the F2 no increase in variance of extra-embryonic fluid was noted.

The effects of two mutant genes were studied. Blebs (my) had no effect on the total fluid in the conceptus, but led to a rearrangement of fluid within the embryo. Brachyphalangy (Xtbph) caused an overall increase in fluid within the conceptus. Distribution of the excess depended upon the phenotype (exencephalic versus non-exencephalic) of the embryo.

In the fungus Podospora anserina, mutations were selected which relieved the hypersensitivity to paromomycin caused by four suppressors assumed to be ribosomal ambiguity mutations (su1–31, su1–49, su1–60, su2–5). Our first purpose was to isolate new antisuppressor mutations and in fact a new antisuppressor gene, AS7 was uncovered. The AS7–1 mutant displays a pleiotropic phenotype and particularly a sporulation defect. On the other hand, a new su1 mutant was obtained which acts as a suppressor and also as an antisuppressor: it can specifically reduce the suppressor effect of certain su2 mutations. This property of some su1 and su2 mutations was already known. Apart from these mutations probably involved in the control of translational fidelity, six mutations conferring cross-resistance to paromomycin and neomycin were isolated. While four of them are localized in the Pm1 and Pm2 loci previously identified, the two others define a new gene which controls paromomycin and neomycin resistance, Pm3. Strains carrying the Pm3–1 allele are sensitive to temperature at the level of growth and sporulation. The three last mutations which were obtained confer no mutant phenotype when separated from the su1 background. They are closely linked to the su2 locus.

Some anomalous results are described of genetical tests using the sex-linked markers Tabby and Bent-tail. The results are shown to be consistent with the demonstration by Welshons & Russell (1959) that the X/O chromosome constitution is female, and suggest that the condition can arise from non-disjunction in the female as well as from non-disjunction in the male parent. A single animal of presumed X/X/y constitution appeared anatomically to be fully male, but died before breeding test could be performed.

Three water-soluble wheat endosperm proteins of the wheat variety Chinese Spring have been shown, by isoelectric focusing, to be the products of genes located on the long arms of chromosomes 7A, 7B and 7D. In the absence of any evidence of function these genes have been assigned the temporary symbol, Wsp-1.

Considerable intervarietal variation was found among a sample of 44 hexaploid wheat varieties. Five alleles at Wsp-A1, three at Wsp-B1 and two at Wsp-D1 were identified. Intrachromosomal mapping showed that Wsp-B1 is located distally on the long arm of chromosome 7B.

Alien homoeoloci were identified on chromosomes 7Hch of Hordeum chilense, 7H of H. vulgare, 7E of Agropyron elongatum, 7S1 of Aegilops sharonensis and 7V of Dasypyrum villosum. Some other loci encoding WSPs found in wheat and some alien species are also briefly described.

The average effect and average excess of a gene substitution are formulated in terms of gene frequencies and inbreeding coefficient. This clarifies their meanings and shows how each is affected by non-random mating. The meanings of various definitions are examined, and one commonly used definition of average effect is found to be invalid with non-random mating. The concept of breeding value is shown to have no useful meaning when mating is not random.