A wild strain of Klebsiella aerogenes (V9A), which contains a plasmid Fklac carrying the genes of the lac operon, gives two mutant cell types, recognized by the appearance of their colonies on MacConkey lactose agar. These are referred to as ML− and ML−/+, wild-type being ML+. ML− cells can grow rapidly on 1% lactose as carbon source but very slowly on 0·2% unless induced by TMG or D-fucose, or by previous growth on galactose, melibiose or raffinose, which enables them to grow rapidly on 0·2% lactose for 2–4 cell generations. Previous growth on 1% lactose does not induce the ability to grow rapidly on 0·2% lactose. It is concluded that ML− cells have a defect in the lactose permease gene which allows slow uptake of lactose when the external concentration is 0·2% and more rapid uptake when the external concentration is increased. In addition, TMG, D-fucose, galactose, melibiose and raffinose induce one or more other galactoside permeases which can accumulate lactose efficiently but are not induced by lactose. ML−/+ cells can grow normally on 0·2% lactose as carbon source, but only after a substantial lag when transferred from glucose, glycerol or sucrose, and after an even longer lag when transferred from melibiose or raffinose. Wild-type cells (ML+) grow normally on 0·2% lactose after a short lag of less than a cell generation time, when transferred from any other carbon source. Cells of each of the three phenotypes (+, −/+ and −) can mutate to give both of the other two phenotypes. Incomplete genetic evidence suggests that the ML− mutation is a result of a reversible change in the Fklac plasmid.

Six lines have been isolated in which individual chromosomes of Ae. umbellulata have been added to the normal complement of T. aestivum. The phenotype and cytology of these lines and of the material employed in their production is briefly described. The use of some of these lines in investigations on the evolution of the diploid Aegilops species and in the introduction of useful alien variation into T. aestivum is mentioned.

Genotypic and phenotypic changes of HCM in P. aeruginosa are due to a variety of causes. In addition to interstrain genetic differences and the semi-permanent effects of growth at 43°C, mutations affecting both restriction and modification have been isolated by direct selection and through the pleiotropic effects of p–fluorophenylalanine resistance mutations. It is suggested that some of these changes affecting HCM may be taking place through alterations of the ribosomes.

The question of what is meant by random fluctuations in selection intensities in a finite population is re-examined. The model presented describes the change in the frequency of a gene in a haploid population of size M. It is assumed that in any generation the adaptive values of A and a are equally likely to be 1 + s: 1 or 1: 1 + s. If s is the selective advantage and x the frequency of gene A, then the first two moments of the change in frequency are found to be m(Δx) = x(1 − x)(1 − 2x) θ/2M and

where E(s2) = θ/M. The ultimate probability of fixation is computed, showing that variability in selection increases the chance of fixation of a rare gene. A more general form for m(Δx) also is obtained. This form is compared with the equation currently used in describing random fluctuations in selection intensities.

An investigation of the genetic aspects of fertility was conducted among inbred and hybrid generations of rats. The high-fertility LEW strain and the low fertility CAS strain were crossed and their hybrids inbred for four generations. Litter size, ovulation rate, sterility, and the weights of the thyroid, pituitary, adrenals, testes, seminal vesicles, ventral prostate, uterus, and ovaries were analysed in inbred and hybrid rats for evidence of strain differences and heterosis and in successive generations of sib matings for inbreeding depression.

CAS females produced smaller litters and had smaller thyroids, pituitaries, adrenals, ovaries, and uteri than LEW females. CAS males had larger testes but smaller adrenals than LEW males. Results of crosses included heterosis for female pituitary and ovary weights, but inbreeding depression for the weights of male adrenals, seminal vesicles, and ventral prostates, and female thyroids and uteri. Ovulation rate did not differ between strains and was not an important determinant of litter size in this study.

The decrease in litter size as a result of inbreeding was due partly to the inbreeding of the parents and partly to the inbreeding of the litter.

Two new sublines of the C57BL/Gr strain of mice have been studied which were derived from earlier sublines in which no genetic variance could be demonstrated. The incidence of some 31 minor skeletal variants was examined which could thus go up or down. As new subline differences have arisen with about the same frequency and mean magnitude of effect as in the past, there is no doubt that, at least in the C57BL strain, subline differentiation is a continuing process. Its high frequency (about 0·01 changes per character at risk per generation) is difficult to reconcile with spontaneous mutation rates of single genes in the mouse. The possibility must thus be considered that some other self-perpetuating processes or entities of some degree of stability are handed down in the lines of descent in which they have arisen, or perhaps become unmasked. There is no reason to suppose that this type of event is confined to inbred strains (in which it can be demonstrated fairly easily); it presumably occurs similarly in mixed stocks in which it would scarcely be detectable.

To evaluate whether sex reversal contributes to sex-ratio imbalance among t6/tw5 double heterozygotes, the cross performed by K. B. Bechtol (Genetical Research 39, 1982, 79–84), T/t6 × T/tw5, was repeated. Significantly more normal-tailed (t6/tw5) females than males were recovered. By contrast, sex ratios were normal among tailless progeny resulting from this cross and among all classes produced by control crosses. Hybridization of a Y-specific DNA probe with genomic DNA from phenotypic females revealed no XY, sex-reversed males. On the genetic backgrounds that generated only moderate transmission distortion of tw5 (81–85%), the overall viability of the doubly heterozygous progeny was only 50% and the sex-ratio skew among this class was strong. However, on a genetic background that displayed extreme tw5 transmission (99%), embryonic viability was more than 80% and the sex-ratio imbalance was weak.

The selective advantage of sexual reproduction is widely regarded as a major unsolved problem in biology. Recently, it has been proposed that the fundamental selective advantage of sex is its promotion of recombinational repair and hence survival of DNA in the germ line of organisms. A bacteriophage T4 system was set up to test this theory. After a phage T4 injects its DNA into an Escherichia coli cell it quickly establishes a barrier, through its immunity function, to infection by a second phage T4, arriving at a later time. This barrier causes phage T4 to reproduce asexually. The immunity barrier has a selective advantage in preserving the host cell as a sole resource for the first phage. If the first phage's DNA is damaged by UV irradiation, however, it has a reduced probability of being able to survive in the host cell when it is there alone. It was found that UV irradiation, in addition to reducing the first phage's viability, also prevents the first phage from raising an effective immunity barrier. This UV-induced reduction in immunity now allows sexual interaction with later-arriving secondary phage or sexual reproduction. It was found that these secondary phage enhanced survival of genes of the UV-damaged first phage. This supports the theory that under DNA-damaging conditions, which should be prevalent in nature, sex would have a selective advantage.

The present study was carried out to examine the genetic mechanism responsible for reversions to fertile phenotype detected in cytoplasmic male-sterile plants of rice. The cms-bo cytoplasm of Chinsurah boro II gave rise to male-sterility in plants without a gametophytic restorer gene (Rf1). Taichung 65 (T65A) was known to be the maintainer which carries no restorer; however, Taichun 65 preserved in our laboratory (T65B) showed partial fertility (about 8% seed set) when crossed with the male-sterile plants. Unexpectedly, the seed fertility gradually increased with repeated selfings and almost fully fertile plants were obtained in the F6 generation. The cytoplasmic substitution lines revealed that reversions to fertile phenotype resulted from mutational events at the nuclear level. The genetic experiments indicated that the partial fertility observed in the F1 hybrid was controlled by a dominant gene, Ifr1, which was carried by T65B. The results obtained suggested that Ifr1 itself was associated with instability of fertility restoration in the presence of cms-bo cytoplasm since partially fertile plants carrying Ifr1 always showed a tendency for gradual increase in fertility in the later generations. The results are also discussed in relation to a rapid genetic change through intensified gametic selection combined with instability.

The mouse X-chromosome controlling elements, detected by their influence on the position effect variegation caused by the X-autosome translocation T (1; X) Ct, have been found to modify the heterozygous phenotypes of two X-linked genes. It is proposed that X-inactivation can be incomplete, the level of inactivation or the frequency of cells in which inactivation is incomplete being dependent upon the ‘state’ of the controlling element located in the X. The data suggest that this is a consequence of a reversal, or partial reversal, of inactivation of the X as a whole in some cells rather than a vairable spread of inactivation along the length of the X.

The effects of two different deletions of the tryptophan operon on the cotransduction linkage of the nearby cysB and pyrF markers were studied using three sets of donor lysates, each produced by a different HT mutant P22 phage strain. Each trp operon deletion (present in both donor and recipient to preserve homology) caused changes in the cotransduction frequencies. This indicated that the HT mutant phage encapsulating mechanism, whose ability to discriminate phage DNA from host-cell DNA is absent or diminished, could still distinguish among nucleotide sequences in selecting bacterial chromosome sites at which to initiate transducing particle formation. The three HT mutant phage strains each produced different sets of cotransduction linkage values, indicating that this aspect of substrate specificity was altered differently and uniquely by each HT mutation.