Plasmid pBR322 is amplified following amino-acid limitation in Escherichia coli relA hosts. In relA+ hosts there was no significant amplification or a much smaller one. Plasmid amplification is due to the relA mutation; when the relA+ allele is transferred into the relA mutant CP79 this strain no longer amplifies plasmid DNA during amino acid starvation. It is concluded that ppGpp is a negative effector of plasmid replication. Amplification is temperature dependent, being maximal at 32 °C and negligible at 37 °C.

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.

In Drosophila melanogaster, the P−M and I−R systems of hybrid dysgenesis are associated with high rates of transposition of P and I elements, respectively, in the germlines of dysgenic hybrids formed by crossing females of strains without active elements to males of strains containing them. Transposition rates are not markedly accelerated in the reciprocal, nondysgenic hybrids. Previous attempts to evaluate the extent to which hybrid dysgenesis-mediated P transposition contributes to mutational variance for quantitative characters by comparing the responses to selection of P−M dysgenic and nondysgenic hybrids have given variable results. This experimental design has been extended to include an additional quantitative trait and the I−R hybrid dysgenesis system. The selection responses of lines founded from both dysgenic and nondysgenic crosses showed features that would be expected from the increase in frequency of initially rare genes with major effects on the selected traits. These results differ from those of previous experiments which showed additional selection response only in lines started from dysgenic crosses, and can be explained by the occasional occurrence of large effect transposable element-induced polygenic mutations in both dysgenic and nondysgenic selection lines. High rates of transposition in populations founded from nondysgenic crosses may account for the apparently contradictory results of the earlier selection experiments, and an explanation is proposed for its occurrence.

The specific activities of α-amylase were measured for two sets of mutation accumulation lines, each set having originated from a different lethal-carrying second chromosome and SM1(Cy) chromosome and having been maintained by a balanced lethal system for about 300 generations. Significant variation was found to have accumulated among lines of both sets. Because of dysgenic crosses in the early generations of mutation accumulation, insertions or deletions of transposable elements in the Amy gene region were suspected of being the cause of this variation. In order to test this possibility, the structural changes in the 14 kb region of these chromosomes that includes the structural genes for α-amylase were investigated by restriction map analysis. We found that most part of the activity variation is due to replacements of a chromosomal region of SM1(Cy), including the structural genes for α-amylase, by the corresponding regions of the lethal chromosomes. One line also contained an insertion in this region but this line has an intermediate activity value. Thus, insertions of transposable elements into the Amy gene region were not found to be responsible for the new variation observed in α-amylase activity. If we remove those lines with structural changes from the analysis, the genetic variance of α-amylase specific activity among lines becomes non-significant in both sets of chromosomes.

We have studied, using light microscopy, the relationship between chromosome content and nuclear diameter in early spermatids of males carrying different combinations of wild-type and compound chromosomes in Drosophila melanogaster. By using these genotypes we have been able to observe spermatid nuclei bearing various numbers of chromosomes ranging from only one sex chromosome and no major autosomes to almost twice the normal chromosome complement. We have found that variations in the chromosome content are accompanied by increasing the variance in early spermatid nuclear diameter; the more gametic classes produced, the higher the variance of nuclear diameters. These results indicate that measuring nuclear diameters in early spermatids represents a useful way to estimate the levels of meiotic non-disjunction and thereby to improve the characterization of lethal or male sterile mutants in which analysis of meiotic chrosome non-disjunction cannot be achieved by conventional genetic methods.

Eggs from reciprocal hybrids between the C57BL/6By and BALB/cBy strains were tested for their susceptibility to attack by hyaluronidase and pronase. There were significant reciprocal differences between the F1 females in the responses of their unfertilized eggs to both enzymes. The F1 hybrids from BALB mothers showed the increased susceptibility characteristic of C57BL whilst the F1 hybrids with C57BL mothers were more resistant to both enzymes, like BALB mice. Eggs from the four kinds of reciprocal F2 hybrid females also showed patroclinous patterns of susceptibility. A patroclinous difference was found between reciprocal crosses of the CXBD and CXBE recombinant inbred strains but not in crosses between recombinant inbred strains with similar phenotypes. Cross fostering did not alter the phenotypes of the C57BL and BALB females or those of their reciprocal F1 hybrids. The findings are interpreted in terms of differential genomic imprinting of paternally inherited information. The possible general usefulness of patroclinous differences between reciprocal F1 females in revealing differences in imprinting is noted.

Complete t haplotypes can be transmitted at distorted ratios from heterozygous +/t male mice as a consequence of t-specific alleles at a series of t complex distorter loci (Tcd-1t through Tcd-4t) and a t complex responder locus. Partial t haplotypes that lack the Tcd-2t allele cannot be transmitted at the very high ratios characteristic of complete t haplotypes. The breeding studies reported here tested the possibility that the absence of Tcd-2t could be compensated for by the presence of double doses of other Tcdt alleles. The results indicate that a double dose of Tcd-4t alone will not work, but that a double dose of both Tcd-1t and Tcd-4t can promote a very high transmission ratio in the absence of Tcd-2t. These results suggest that the extent to which transmission ratios are distorted is dependent upon the absolute level of expression of the individual Tcd genes. Further studies of genotypic effects on transmission ratio distortion, as well as fertility, lead to the suggestion of a fifth t complex distorter (Tcd-5) locus within t haplotypes.

Parental imprinting effects for chromosome 16 were investigated using disomic animals which were obtained by mating (Rb32Lub × Rb2H) F1 mice. Two allelic forms of the enzyme CuZn-superoxide dismutase, Sod-1a and Sod-1c, were` used to identify maternally or paternally disomic animals. Both types of disomic animals were found with the expected frequencies and did not visibly differ from one another or from non-disomic animals. These results indicate that the genomic imprinting mechanism either does not act on chromosome 16, or, if it does, does not do so in a manner which affects normal development.

DNA sequencing and restriction mapping provide us with information on DNA sequence evolution within populations, from which the phylogenetic relationships among the sequences can be inferred. Mutations such as base substitutions, deletions, insertions and transposable element insertions can be identified in each sequence. Theoretical study of this type of sequence evolution has been initiated recently. In this paper, population genetical models for sequence evolution under multiple types of mutation are developed. Models of infinite population size with neutral mutation, infinite population size with deleterious mutation and finite population size with neutral mutation are considered.