A mutant (Mb-s) of Escherichia coli K12 which is more sensitive than wild-type (Mb-r) to such dyes as methylene blue or acridines was studied. The Mb-s mutant can also be disinfected of F factor with lower concentrations of acridine orange than Mb-r bacteria. The Mb locus was mapped by crosses between Hfr and F−, F-duction with F13, and transduction with phage P1. It was found to be situated between the pur and T6 loci on the chromosome. Moreover, it was found to be contained in the chromosomal fragment carried by the F-prime, F13. In a heterogenote obtained by F-duction, the Mb-r gene is dominant over the Mb-s gene. The Mb gene was transduced jointly with the pur gene by phage P1.

Previous measurements of specific locus mutation rates in mice had all involved the seven loci, a, b, c, d, p, s and se. An experiment was performed with the same mouse stock (C3H × 101) and the same radiation dose (600 rad) to spermatogonia as had been used previously, but employing a new group of six loci, a, bp, fz, In, pa and pe. The observed mutation rate, 5·0 × 10−8 per locus per rad, was significantly lower than that for the original seven loci, but was three to four times higher than the corresponding mutation rate in Drosophila melanogaster.

Five allelic mutants of Neurospora which lack glutamic dehydrogenase (am mutants) were induced to revert with ultra-violet. The glutamic dehydrogenase produced by the revertants was compared to that of wild-type. Several distinct classes of revertants could be distinguished by these tests. However, genetic analysis showed that all the reversions resulted from events at or near the site of the original am mutation. The spectrum of reversion types depended on the nature of the am mutant employed. One mutant, which produces an am protein believed to be altered in its active site, yielded revertants which were all indistinguishable from wild-type. Another mutant, which produces a protein with a functional active site but altered folding properties, gave at least six classes of revertants which were different from wild-type.

A mouse antigen, MuB1, has been shown by the study of backcrosses to be inherited in a unifactorial dominant manner. Its inheritance is not linked with gamma globulin allotypes, but has been shown to be linked with the presence of the haemolytic complement system. The concentration of MuB1 in the serum of several inbred strains of mice showed sex-associated differences; however, the presence of MuBl did not depend on the sex of the parents or on the sex of the offspring. The inheritance of antibody responsiveness is discussed in terms of the inheritance of the antigen, MuB1.

The pattern of changes of the genetic covariance between two characters on selection was examined in an effort to explain the asymmetry of correlated responses in two traits, or of the same trait in two environments, frequently observed in experimental results.

The algebraic conclusions were further examined by model selection experiments using a computer. The computer was programmed to calculate the change in gene frequency from generation to generation and to calculate from it the expected changes in genetic variances and covariance as selection proceeded. This procedure was carried out with several models of gene effects and gene frequencies.

Asymmetry of the genetic covariance, and consequently of the correlated responses, resulted when the relative change in gene frequency at the loci contributing positively and negatively to the covariance depended on the trait selected. The conditions necessary for the development of asymmetry were examined and the results suggest that any symmetry found in an experiment is perhaps more surprising than asymmetry. Probably the most frequent contribution to asymmetry in practice will be from loci contributing negatively to the covariance and having frequencies other than 0·5.

Accurate prediction of correlated response over many generations is therefore not possible without prior knowledge of the composition of the genetic covariance, as well as its magnitude. The validity of existing theory for the prediction of correlated responses is likely to be much poorer than for the prediction of direct responses. Predictions would then have to be based on the genetic parameters estimated in each generation.

A review is given of published accounts of mosaics in mice and other rodents, of mutations and of certain unexplained events. The cumulative weight of evidence makes a strong case for the existence of somatic crossing over in the laboratory rodents.

A survey of past work shows that certainty in the electrophoretic classification of mouse haemoglobins requires further understanding of the meaning of the multiple electrophoretic bands observed.

Six electrophoretic bands are observed in all. Numbered in order of mobility they give the formulae 2 for Hb-s, 1235 for Hb-d, 1246 for Hb-p and 12345 for foetal haemoglobin (Hb-f). When mercaptoethanol is added to the electrophoretic medium these formulae become: 2 for Hb-s, 23 for Hb-d, 24 for Hb-p, 234 for Hb-f. Bands 5 and 6 and a fast ultra-centrifuge fraction both increase when samples are stored.

Bands 5 of Hb-d, 6 of Hb-p, and probably 5 of Hb-f, are dimers of the whole haemoglobin molecule almost certainly joined by sulphur bridges. The monomers are bands 2 and 3 of Hb-d and 2 and 4 of Hb-p. Within each type interconversion of bands 2 and 3 and bands 2 and 4 has been observed.

The hypothesis is suggested that Hb-d and Hb-p both exist as two conformational isomers. In each case one isomer is electrophoretically indistinguishable from Hb-s: the other permits the electrophoretic recognition of their differences in bands 3 and 4, and the formation of sulphur bridges to give bands 5 and 6.

Curtailed (Tc) is a new T-allele which leads to complete or near-complete absence of the tail in heterozygotes, apart from a small caudal filament. Other heterozygous defects include absence of the axis odontoid process and of the nuclei pulposi, a tendency to have rib and vertebral fusions and a slight decrease in the average number of presacral vertebrae. Tc is lethal when homozygous, causing similar but more extreme defects than T, with absence of all limb-buds and non-closure of the neural folds. A comparison of Tc with other mutants suggests that the anomalies are mainly the result of more severe effects on the notochord-mesoderm system than in T. Differences between the genetic behaviour of T, Tc and Th are discussed.

1. This paper describes further investigations of the high sternopleural chaeta-number lines of Drosophila melanogaster established by directional selection by Thoday & Boam (Genet. Res. 2, 161). The lines are vg 4 with a mean of 35·6 and vg 6 with a mean of 39·2 chaetae per fly.

2. Two locatable polygenes, 3a and 3b, distinguish the line third chromosomes from those of Oregon inbred (mean about 20·5, an ancestor of all the lines). These two genes are both located between the markers h and eyg and do not interact.

3. There is one locatable polygene at 41·1 ± 1·7 centiMorgans distinguishing the line second chromosomes from those of Oregon. There is no evidence that this gene is a linked complex, and, if it be a linked complex, it is unlikely to occupy more than 2 map units of the second linkage group. It interacts strongly and positively with the gene 3a.

4. These three genes account for 80% of the genetic variance of the vg 4 × Oregon F2.

5. Two separate regions at 2·4 ± 0·5 and 50·5 ± 0·9 centiMorgans distinguish the vg 6 × chromosome from that of Oregon. They do not appear to interact. Together they interact strongly and positively with gene 3a.

6. These five genes account for 87·5% of the chaeta-number difference between vg 6 and Oregon.

7. The locatable polygenes on chromosomes II and III each have qualitatively distinguishable developmental effects.

8. It is pointed out that, though the genetics of these lines may be unusually simple, the results indicate that attempts to locate specific genes and study their individual effects should be made more often by students of continuous variation. Since the location of the polygene in chromosome II was done using marker genes 45 map units apart, such studies may be practicable even in species whose linkage groups are much less well marked than those of Drosophila melanogaster.

Data from three experiments bearing on the relative stability of the four mating systems required to test the restrictions against inbreeding and unequal family size were examined in relation to the results given by Robinson & Bray (1965). Tribolium castaneum was the experimental animal used in these experiments.

An analysis of variance indicated that both restrictions were probably effective (P approximately 0·10) in reducing the phenotypic variability of control population means. It seems likely that the apparent gain in stability obtained when the inbreeding restriction was used in addition to the restriction against unequal numbers is due to non-random genotypic proportions which would affect estimates of genetic variability based on assumptions of random mating.

The locus of the gene striated, Str, on the mouse X-chromosome, was previously reported to be on the side of tabby (Ta) away from bent-tail (Bn). Results given in the present paper show this report to have been incorrect, and that the order of loci is Bn-Str-Ta-(Mo-Blo). In addition, the position of the translocation break in Searle's translocation (T1GH) has been confirmed, the order of loci with respect to T16H being Bn-T16H break-Ta-Blo.

The genetic elements promoting conjugation associated with transmissible drug resistance are of two or more kinds. Experiments with phage specific for F+ bacteria have shown that one large class differs from F essentially only in the production of a cytoplasmic repressor which limits the synthesis of the specific F pilus, whether by the RTF itself or by F when this is present in the same cell.

The sex factor F is itself exceptional among conjugation factors in being freely expressed in all the bacteria of a culture, while related factors which are largely unexpressed are widespread. These can be recognized by the presence of a small proportion of cells sensitive to phage specific for F+ bacteria, and may sometimes constitute the conjugation factors associated with colicinogeny. Moreover, F itself can mutate to the repressed state so that derivatives of E. coli K12 which appear F− include some in which F is still present but rarely expressed.