Curing of an F-prime plasmid by imipramine was most efficient on bacteria growing semianaerobically at 37 °C. The plasmid curing effect of imipramine was increased in the presence of methylene blue, whilst fluorescein, chlorpromazine-sulphoxide and tetraoxyanthrachinon antagonized the plasmid curing action of the drug. In addition to its plasmid curing effect, imipramine treatment selected for Lon mutants at high frequency. Lon mutants show increased resistance to the drug but cured strains, if Lon+, are not resistant.

This paper provides direct evidence for the occurrence of mitotic crossing-over in leaf tissues and in vitro cell cultures of Nicotiana tabacum. The geno-typic composition of both segregating regions of twin spots was analysed by in vitro culture of the segregating tissue and by regenerating plants from this tissue. The frequency of mitotic crossing-over is influenced by several physical and chemical agents.

Mouse t haplotypes have been divided into nine subregions that are each defined by one or more molecular markers. In previous studies, three of these subregions were shown to contain ‘distorter loci’ that interact to effect the transmission-ratio distortion phenotype characteristic of all complete t haplotypes. To determine which of the remaining six subregions also play a role in this phenotype, we analysed the accumulated data on transmission ratio distortion from males that carried one of 26 different combinations of two partial t haplotypes. We have obtained evidence for the association of two additional subregions with distorter loci. First, we present further evidence for the existence of a previously postulated distorter locus, Tcd-3, and describe its mapping to the T66C subregion. Secondly, we describe the identification of a new distorter locus, Tcd-4, in association with the subregion defined by the structural gene for the TCP-1 protein. Further studies indicate that two doses of the Tcd-4 locus are equivalent in effect to a single dose each of Tcd-4 and a second distorter locus, Tcd-1. This result suggests that different distorter locus products could have a common mode of action.

The properties of two transfer-deficient Flac mutants (in Escherichia coli K12) carrying mutations in the cistron traL are described. The traL product is needed for conjugational DNA transfer and for pilus formation, but not for surface exclusion; it is not plasmid-specific. traL maps between traA and traE; one of the traL mutations is apparently polar on traA. The properties of Tra+ revertants of this mutation suggest that the traL product is directly required for F-specific phage infection.

Evidence from a functional analysis of host-specificity mutants in merodiploids is presented which supports the suggestion that three genes, hss, hsr and hsm, are necessary for the expression of host-controlled restriction and modification. The host-specificity phenotype expressed by the merodiploids provides evidence that at least two genes, hss and hsr, are concerned in the expression of host-specific restriction of DNA and one of these genes, hss, is responsible for the strain specificity of the restriction enzyme. A class of modification-deficient mutants isolated from restriction-deficient, modification-proficient mutants, was also tested for complementation in merodiploids and the phenotype of these merodiploids provides evidence that at least two genes, hss and hsm, are concerned in the expression of host-specific modification of DNA and one of these genes, hss, is responsible for the strain specificity of the modification enzyme. How these three genes function at the molecular level is discussed in terms of models based on the interaction of subunits to form oligomeric enzymes.

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.

In marsupials, X chromosome inactivation is paternal and incomplete. The tissue-specific pattern of inactivation of X-linked loci (G6PD, PGK, GLA) has been attributed to a piecemeal inactivation of different regions of the X. We here propose an alternative hypothesis, in which inactivation of the marsupial X is a chromosome-wide event, but is differentially regulated in different tissues. This hypothesis was suggested by the relationship between the positions and activity of genes on the kangaroo paternal X. In the absence of an HPRT polymorphism, we have used somatic cell hybridization to assess the activity of the paternal HPRT allele in lymphocytes and fibroblasts. The absence of the paternal X, and of the paternal forms of G6PD or PGK, from 33 cell hybrids made by fusing HPRT-deficient rodent cells with lymphocytes or fibroblasts of heterozygous females, suggests that the HPRT gene on the paternal X is inactive in both tissues and therefore not selectable. Since HPRT is located medially on the Xq near GLA, which shares the same characteristics of activity, we suggest that the locus-specific and tissue-specific patterns of activity result from a differential spread of inactivation from a single control locus, located near HPRT and GLA, outwards in both directions to G6PD and PGK. The nucleolus organizer region on the short arm does not seem to be part of the inactivated unit.

Growth relations of lines selected for fast or slow larval feeding rate have been compared with those in the genetically heterogeneous control base population from which they were derived. Larvae of the slow strain have reduced growth rate and reach their critical weight for pupation later than unselected larvae. Larvae of the fast strain attain their critical weight at the same time as the unselected control larvae, suggesting that growth rate in the precritical period of development is already maximized in the base population and cannot be improved by increasing food intake. This constraint does not apply to the fixed period of post-critical growth however, since fast feeding larvae give rise to larger adult flies than the controls.

Larval feeding rate is affected by genes located on all three major chromosomes. The small fourth chromosome has negligible effect. Selection for slow feeding rate has led to an increase in the frequency of recessive genes affecting the character. High scores of larvae selected for fast feeding rate depend upon interactions between non-homologous selected chromosomes which individually have little effect. Larval feeding rate in the control unselected population appears to be buffered, firstly by epistatic interactions against the effects of chromosomes tending to promote ‘supra-optimal’ feeding rate and, secondly, by dominance against chromosomes promoting a lowering of feeding rate.

Under conditions of scramble type competition between the selected lines for limited resources, fast feeding larvae have a higher survival rate, and complete their period of larval development earlier to give larger adult flies than their slow feeding competitors. The contribution of larval feeding rate to competitive ability at different levels is discussed, and it is suggested that the effects of change in this behavioural character may be far reaching.

Incidence of colourblindness among 3325 males belonging to 21 endogamous Dhangar castes (shepherds) of Maharashtra, India, has been reported. Of the 21 castes studied 5 lacked the gene for colourblindness, while in other groups it varied from 1% to 55%, with a series average of 2·65%. The low incidence of observed colourblindness has been discussed in the light of the nomadic way of the life of some of the Dhangar castes. The results have been compared with other nomadic populations of Maharashtra. The results, in general, are compatible with the Post and Pickford's hypothesis of differential selection for colourblindness.

Epididymal sperm from male mice carrying tw32 (t12 complementation group) exhibit a peculiar nonprogressive type of motility called ‘dancing’; sperm from congenie wild-type mice do not. To determine whether this effect was unique to tw32 or common to all t haplotypes, sperm from mice carrying other t haplotypes were examined. A male was considered to have nonprogressive sperm if more than 20% of the motile sperm had nonprogressive trajectories. The mean percentage of nonprogressive but motile sperm for 33 wild-type and Brachyury males of various genetic backgrounds was 4. All males carrying tw12 (tw1 complementation group), tw5 or tw73, and 56% of males carrying t0 or tLub1 had nonprogressive motile sperm. Five per cent of males carrying t chromatin or a deletion in the proximal (to the centromere) half of the t complex had nonprogressive motile sperm, but all males carrying t chromatin in the distal half of the t complex had nonprogressive motile sperm. These observations suggest that the factor or factors causing nonprogressive sperm motility may be common to all complete t haplotypes, and located in the distal region of the t complex.

N-methyl-N′-nitro-N-nitrosoguanidine treatment of a donor strain of Pseudomonas aeruginosa resulted in the isolation of strains which were presumably cured of their sex factors, strains which possibly contained mutant defective sex factors and one strain which showed enhanced donor activity. The latter was apparently due to a change in the bacterium and the sex factors of OT 302 and OT 15 were both shown to be similar to the original in OT 1 when the three were transferred into the same strain.

Mutations in five loci that modify the phenotype of whiteapricot (wa), caused by the retrotransposon, copia, were examined in two-way combinations to determine whether their effects were additive or epistatic. All two-way combinations of mutations in these five loci, mottler of white (mw), suppressor of forked (su(f)), suppressor of white apricot (su(wa)), Enhancer of whiteapricot, (E(wa)) and Darkener of apricot (Doa), are additive in their effects on wa, implying that each second-site modifier locus affects a different process. Three other copia-induced mutations, HwUa, whd81b25 and ctns were also examined for responsiveness to mutations in these modifier loci. None clearly responded. Mutations associated with B104 insertions, including Gl, vgni, ctn and wric were also examined for responsiveness to mw mutations, which have specificity for this element as well. Both vgni and wric respond to mutations in mw. The former interaction demonstrates that mw is capable of interacting with B104 elements in loci other than white. The significance of the results with respect to the nature of second-site modifier loci is discussed.

A method is described for detecting centromere linkage in Saccharomyces cerevisiae using a simple monohybrid for the locus in question. The method utilizes the two-spored asci produced by a normal homothallic diploid and depends upon a selective elimination of specific chromatids during spore formation. The pattern of selective elimination was not detected in a heterothallic strain but was found to be a dominant trait in an inter-strain cross. It was shown that gross chromosome aberrations are probably not responsible for the two-spored asci produced by either the heterothallic or homothallic strains.