The sex factor of colE1a appears related to Ib, the sex factor of colIb, by each of three criteria: mutual inhibition of epidemic spread, antigenic structure of the sex pilus and susceptibility to I phage. The failure of each factor to spread in cultures carrying the other implies that donor ability is subject to a cytoplasmic repressor. Unlike two colI factors, colE1a and colIa (or Ib) can co-exist to give a doubly colicinogenic strain.

Contrary to what their name asebia implies, mice homozygous for the ab gene do possess actively secreting sebaceous glands which develop normally from the follicular outer root sheath, at 18 days post-conception. However, by the 20th day post-conception, these mice exhibit the abnormal sebaceous cytodifferentiation which remains typical of the asebic glands throughout life. Nests of outer root sheath cells below the sebaceous glands also undergo atypical sebaceous differentiation. The smooth membrane system and mitochondria, which appear to be responsible for the orderly accumulation of lipid droplets and sebum production in normal mice, become increasingly abnormal in asebic mice. Fewer lipid droplets form, the smooth endoplasmic reticulum becomes distorted and dilated, and the normal transformation of mitochondria does not occur. Atypical differentiation occurs randomly and ‘differentiated’ cells often degenerate within the asebic sebaceous glands. Of the larger specialized sebaceous-type glands studied, only the Meibomian glands are similarly affected by the asebia mutation, while the anal and preputial glands appear to undergo a more normal cytological differentiation. The abnormalities seen in the asebic sebaceous glands seem to be due to defective regulation of the synthetic or degenerative processes necessary for completion of normal sebum production. Both the defects of sebaceous glands and the unusual characteristics of the epidermis and hair follicles in asebic mice may be initiated by the abnormal underlying dermis or the apparently abnormal endocrine system.

Previous studies have shown that the mouse X chromosomal locus, Xce, which causes non-random X chromosome inactivation, is closely linked to the Is(X; 7)Ct X-autosome translocation. This has placed it either near Ta on one side of the breakpoint or near jp on the other. Linkage tests with Movbr and Ta now demonstrate that the locus in fact lies close to Ta. The data also provide genetic evidence which establish that the C3H/HeH X chromosome carries the Xcea allele of this gene and the JU/FaCt and C57BL/GoH X chromosomes carry the Xceb allele, and further suggest that the X-linked modification of the heterozygous phenotypes of X-linked genes observed by various other investigators are all attributable to differences at the Xce locus. Evidence of a maternal influence upon Movbr phenotypes is also presented. This appears to operate independently of the X-inactivation process, probably through an effect of differing levels of copper in the milk in early life upon the mutant coat colour in the young.

A study of the gene B6m, previously described as a modifier, revealed that it is a recessive resistance gene of moderate effect when homozygous. Its value in enhancing resistance to bacterial blight when in combination with other genes, in particular B2, is emphasized. The symbol for the gene is simplified to B6.

Euploid and aneuploid plants of Triticum aestivum, variety Chinese Spring were pollinated with, pollen of Hordeum bulbosum. Euhaploids and aneuhaploids of Chinese Spring were obtained from the crosses. Meiotic chromosome pairing was analysed in 25 different aneuhaploids and the results were compared with those obtained from euhaploids. The evidence provided by the meiotic studies was used to identify chromosomes whose activities affected the genetic control of chromosome pairing.

Meiosis was abnormal in a 23-chromosome aneuhaploid and in the 22-chromosome sectors of a chimaeral plant. Both plants were thought to have resulted from the incomplete elimination of the genome of H. bulbosum from hybrid embryos. It is suggested that the meiotic abnormalities in the two aneuhaploids were caused by the residual barley chromosomes.

Twenty-four mutants of Aspergillus nidulans were isolated which grew more slowly than normal on glucose as sole source of carbon and were unable to utilize intermediates of the tricarboxylic acid cycle. By complementation tests they were divided into five groups, each group representing a different cistron and the cistrons were assigned to linkage groups by mitotic analysis. The mutant loci have been designated sgp-1 to sgp-5 respectively. Three mutants have been mapped by meiotic analysis.

Argininosuccinase has been purified from wild-type Neurospora crassa, strain ST.A. The purified enzyme, which is homogeneous by the criteria of analytical centrifugation and starch-gel electrophoresis, has a molecular weight of about 175,000. The enzyme has also been partially purified from a heterokaryon between the arg-10 mutant stocks B317–9–9a and 402–3a.

The reaction kinetics of the two enzymes were compared in several respects, and they were found to be indistinguishable. The enzymes were also indistinguishable by starch-gel electrophoresis, and sedimented at the same rate through a sucrose gradient. It seems likely, however, that the enzymes do differ physically since they showed different affinities for both calcium phosphate gel and hydroxylapatite during purification.

The functional morphology and the replication pattern of the male X-chromosome in an autosome-X insertion stock (T(1;3) 05) of Drosophila melanogaster have been examined. In larval salivary glands carrying this insertion neither the enlargement and pale staining of the single male X, nor the characteristic early completion of replication cycle, as revealed by 3H-TdR autoradiography is in any way changed. The normal properties of the inserted autosomal segment are also unaltered. The results appear to support a ‘piecemeal’ type of dosage compensation mechanism in Drosophila operating through the male.

The order of replication of a series of genes in Pseudomonas aeruginosa has been studied in synchronized cultures using a method based on the technique of sequential mutagenesis. This technique relies on the increased susceptibility of the replication point of the bacterial chromosome to mutagenesis by N-methyl-N′-nitro-N-nitrosoguanidine. The genes studied were those previously mapped by conjugation and whose order of replication had been studied by an investigation of gene frequencies in exponential populations. The results are consistent with the idea that there is two-way replication of the chromosome of P. aeruginosa starting at a point near trp-1 and arg-6. They also confirm that the two linkage groups which have been found by conjugation replicate at different times. If the assumption is made that there is only one chromosome in P. aeruginosa, the results can be used to show how the two linkage groups may possibly be joined together and the order is such that there would have to be two sites of attachment for the sex factor FP2.

Breeding stocks were re-established from embryos of various mutant and inbred strains of mice after prolonged storage in liquid nitrogen at the 8-cell stage even with strains where only a proportion of the progeny were of the desired type, i.e. in the ModP and XO strains. Gonadotrophin treatment failed to produce superovulation consistently in any of the strains tested. Although the initial survival of embryos after thawing and culture to the morula and blastocyst stage was highest for embryos from XO mothers (61%), these embryos suffered the heaviest early postimplantation loss after transfer (61%). The proportion of embryos, originally frozen, developing into foetuses and offspring was variable (13% HT, 14% PT, 20% ModP, 14% XO, 21% CBA and CBA-T6) and lower than previously reported for hybrid 3H1 embryos (20–30%). The sex ratio of the liveborn young was within the normal expected limits except for the Modp strain, where it differed significantly from the exected 2♂:1♀ ratio. The proportion of young of the desired type from the frozen embryos of Modp and XO females was less than expected (17 and 3% respectively). In all cases a normal breeding stock was reestablished whose performance was within normal limits for each strain. Even without further improvements in embryo collection and the freezing technique per se, the storage of embryos in liquid nitrogen is an extremely economic way of preserving mouse genetic stocks.

Susceptibility to urethane-induced lung adenomas in mice has a polygenic mode of inheritance, with no obvious discontinuity in lung tumour counts among 37 AXB recombinant inbred strains. However, mean tumour counts were markedly higher in strains carrying the A/J allele at the Kras2 and H2 complex than in those carrying the C57BL/6 allele. In 162 F2 hybrids and small numbers of both backcrosses between strain A/J (susceptible) and C57BL/6 (resistant) mice, five factors influencing susceptibility were identified. Variation due to the ‘major’ Kras2 locus (chromosome 6) accounted for 60% of the total variation. ‘Minor’ loci linked to microsatellite markers Tnfb (in the H2 complex), D9Mit11 and D19MH16 (on chromosomes 17, 9 and 19, respectively) accounted for a further 13% of the variation, and males had more tumours than females with sex differences accounting for 2% of the variation. No significant association with 32 other loci was detected. On a square-root transformed scale, heterozygotes at all marker loci were of intermediate susceptibility compared with homozygotes. Thethree minor loci and sex only affected lung tumour counts when at least one susceptible Kras2 allele was present.

1. Inheritance of flower colour in Delphinium ajacis is controlled by a locus with three stable alleles: pb (blue) is dominant to pl (lavender), which is dominant to p (pink). An unstable allele, p*, exists in a number of states, distinguished by the pattern of their mutation to pb and p during the development of the sepals.

2. The rate of occurrence of blue sectors and spots in the developing sepals of p*p* plants is twice that in the sepals of p*pl plants. The rate of mutation to pb apparently falls during the development of the sepals and this is probably due to p* mutating also to the stable p allele.

3. The frequency of pb and p gametes from p*p* plants is twice that from p*pl plants.

4. The pb mutants from p* show no evidence of instability; the controlling element has transposed from the locus.

5. Some p mutants from p* are apparently stable; others can reacquire instability, especially during sexual reproduction. The latter are tentatively interpreted as due to transpositions of the controlling element to other sites within the gene.

6. The instability of p* is only shown in the presence of a dominant activator.

7. Evidence is presented of transposition of the controlling element from p* to a locus controlling the colour of the foliage.

We have investigated a mathematical model of the process of activation of the X chromosomes in eutherian mammals. The model assumes that the activation is brought about over some definite time interval T by the complete saturation of N receptor sites on an X chromosome by M activating molecules (or multiples of M). The probability λ of a first hit on the receptor site is considered to be very much lower than that of subsequent hits; that is, we assume strong co-operative binding. Assuming further that an incomplete saturation of receptor sites is malfunctional, we can show that for proper activation of X chromosomes in normal diploid males and females, we must have λMT ≥ 3 and 0·96 ≤ N/M ≤ 1. An extension of this analysis for the triploid cases shows that under these conditions, we cannot explain the activation of two X's if the number of activating molecules is fixed at M. This suggests that there must be two classes of triploid embryos differing from each other in a step-wise manner in the number of activating molecules. In other words, triploids with two active X chromosomes would require 2M activating molecules as opposed to M molecules in triploids with a single active X. This interpretation of the two classes of triploids would be consistent with differing imprinting histories of the parental contributions to the triploid zygote.