Starvation for isoleucine inhibits chromosome, minichromosome and pBR322 DNA replication in a stringent strain of E. coli, but does not do so in a relaxed mutant. Starvation for other amino acids inhibits either chromosome and minichromosome replication in both strains. From these results we conclude that oriC and pBR322 replication are stringently regulated and that isoleucine seems not to be essential for the protein synthesis required at the initiation of oriC replication. Deprivation of isoleucine in a Rel− strain gives rise to amplification of minichromosome and pBR322 with a better yield of the latter plasmid than that following treatment with chloramphenicol.

We have investigated the effect of the ribosome-targeted antibiotic kasugamycin (ksg) in Podospora anserina. While ksg inhibits both growth and sporulation, it has a stronger inhibitory effect on the sporulation process. It was previously reported that sporulation of Podospora could be impaired when ribosomes translate with a too high accuracy, and since ksg was demonstrated to increase the ribosomal accuracy in E. coli, we wondered whether it would act similarly in Podospora. As a first approach we have isolated two mutations at different loci, Ks1 and Ks2, that increase the resistance to ksg at the level of both growth and sporulation. Interestingly Ks1−1 also confers a decreased resistance to paromomycin, which is a mistranslation inducer. Characterization of Ks1−1 and Ks2−1 mutants suggests that they could be ribosomal mutants.

DNA reassociation kinetics were used to determine the amounts and organization of repetitive and unique DNA in four mosquito species: Anopheles quadrimaculatus (Say), Culex pipiens (L.), Aedes albopictus (Skuse) and Ae. triseriatus (Say). Intraspecific variation in repetitive DNA amounts was examined in two geographic strains of Ae. albopictus fom Calcutta, India and the island of Mauritius. Repetitive and unique sequences in An. quadrimaculatus were distributed in a pattern of long period interspersion. Repetitive DNA in all other mosquito species exhibited a pattern of short period interspersion. The amounts of fold-back, middle repetitive, and highly repetitive sequences increased with genome size. The amount of foldback DNA increased at a much slower rate than the middle and highly repetitive sequences. Intraspecific variation in genome size in Ae. albopictus was due primarily to the amounts of highly repetitive DNA. S1 nuclease digestion of repetitive DNA in all species revealed a positive correlation between genome size and the proportion of the repetitive DNA consisting of short repeats. The amounts of long and short repeats increased with genome size but short repeats increased at a higher rate. The repetitive DNA of the Mauritius strain contained approximately 15% more short repeats than the Calcutta strain. These findings suggest that genome evolution in mosquitoes has resulted from changes in both the amounts and organization of repetitive elements.

The chromosomal region surrounding the ed, dp and cl genes has been studied cytogenetically (24–26 on 2L chromosome). It contains three Minutes and a haplo-sterile function. For isolation of deficiencies and mutations these haplo-insufficient functions were covered by an insertional translocation of 24D4-25F2 into the X chromosome, or by tandem duplications. 112 lethal and visible mutations induced by EMS and X-rays have been localized by deficiency mapping to 20 subregions. They specify 42 loci in a 48 band interval consistent with the notion that most of the bands encode a single lethal function. The dp, DTS, tkv and suppressor/enhancer loci for position-effect variegation were studied in detail. A dominant suppressor function was localized within the structural part of the dp complex. New non-conditional lethals have been isolated for the DTS locus. Complementation analysis with the previously identified dominant heat-sensitive alleles places the site for heat sensitivity in the middle of the locus. Two haplo-abnormal enhancers of position-effect variegation were localized in the region 25F2–26A1. A triplo-abnormal suppressor function maps to 26B2–5; 26B9. The dose-dependent functions of these loci were studied by the use of deficiencies and duplications.

The ribosomal RNAs produced by the multigene families on the X and Y chromosomes of Drosophila melanogaster are very similar despite the apparent evolutionary isolation of the X and Y chromosomal rDNA. X–Y exchange through the rDNA is one mechanism that may promote co-evolution of the two gene clusters by transferring Y rDNA copies to the X chromosome. This hypothesis predicts that the proximal rDNA of X chromosomes will be Y-like. Consequently, rDNA variants found only on the X chromosome (such as those interrupted by type 1 insertions) should be significantly clustered in the distal X nucleolus organizer. Proximal and distal portions of the X chromosome nucleolus organizer were separated by recombination between the inverted chromosomes In(1)scv2 (breakpoint in the centre of the rDNA) and In(1)sc4Lsc8R (no rDNA). Molecular analyses of the resulting stocks demonstrated that rRNA genes containing type 1 insertions were predominantly located on the chromosome carrying the distal portion of the X rDNA, thus confirming a prediction of the X–Y exchange hypothesis for the co-evolution of X and Y chromosomal rDNA. Distal clustering is not predicted by the alternative hypotheses of selection or gene conversion.

With 12 alleles at the Est-α locus of Drosophila virilis, 44 genotypes of females heterozygous for a pair of them were constructed, and about 4 × 104 of their F1 progenies per genotype were electrophoretically examined. Eighty-three variants different from both of their parental alleles were obtained from a total of 2·0 × 106 progenies. Statistical analysis suggested most of their variants to be recombinants. And no null or inactive allele, of which frequency is several percent in natural populations, appeared in 11·6 × 104 progenies from females heterozygous for active alleles. These results suggest that the high variation of the Est-α locus in this species is generated by recombinants from female heterozygotes.

To analyze abnormal fertilization in a hereditary mosaic strain (mo/mo) of Bombyx mori, the percentages of diploidy mosaic, polyploidy mosaic and polyploid eggs in a batch were estimated by using egg colour mutants (pe re). Among 48 890 eggs from crosses of pe + / + re, mo/mo females with pe re/pe re males, 9409 abnormal eggs were obtained; 4472 of them were diploidy mosaics (red-white eggs), 4038 were polyploids (black eggs) and 899 were polyploidy mosaics (566 black-white, 256 black-red and 77 black-white-red eggs). The total number of diploidy mosaic eggs was approximately equal to that of polyploid eggs. A significant correlation was detected between the diploidy mosaic and polyploid egg ratios within a batch. This suggests that diploidy mosaics are produced by double fertilization in which two genetically non-identical egg nuclei are fertilized in turn by a sperm, and polyploids are formed by the fertilization of a diploid, non-disjunctive egg nucleus gamete by a single sperm. Our results also indicated the presence of common factors modifying both mosaic and polyploid frequency. The concordance of the observed ratio of polyploidy mosaic eggs (1·84%) with the expected value (diploidy mosaic ratio × polyploidy ratio × 2 = 1·83%) suggests that the formation of mosaics occurs independently of the formation of polyploids in this abnormal fertilization process. We point out that it is necessary to modify Goldschmidt & Katsuki's general model to explain abnormal fertilization, and we propose several possible models.

Dysgenic and non-dysgenic base populations were made by reciprocal crossing of Harwich (P) and Canton-S (M) strains. From each cross, two up and two down selection lines were established, with selection on abdominal bristle number for ten generations. The intensity of selection was 10 out of 50 individuals from each sex. Mean bristle number, phenotypic variation and heritabilities were compared between dysgenic and non-dysgenic populations under selection. Except for an anomalous non-dysgenic downline in which a mutation of large effect occurred, all lines showed similar responses to selection. These results contrast with the results reported by Mackay (1984, 1985) in which substantial increases were obtained for response to selection, phenotypic variation and heritability in the dysgenic compared to non-dysgenic lines. There are some indications that the higher response in our aberrant non-dysgenic downline is the result of transposition. Possible explanations for the occurrence of transposition and dysgenesis in the lines derived from nondysgenic crosses are discussed.

The sex-reversal mutation, Sxr and a variant form, Sxr′ have been established on the inbred C57BL/6Mcl background by repeated backcrossing to form the CB and CB′ strains, respectively. DNAs of normal XY, XX Sxr and XX Sxr′ as well as XY Sxr and XY Sxr′ carrier male mice have been digested with the restriction enzymes Hae III and Hinf I and electrophoresed. The DNAs show many common but also differing hybridization bands with synthetic oligonucleotide probes. In XY Sxr (and XY Sxr′) carrier males, the hybridization patterns of normal XY and those of XX Sxr (and XX Sxr′) males are simply superimposed. Individual differing bands can be categorized by their differential hybridization behaviour to the (GATA)4, (GACA)4, (GATA)2 GACA (GATA)2 and (GATA)3 (GACA)2 probes. In general, the hybridization patterns are regularly inherited. In addition to the predominant pattern in each strain, one additional XX Sxr and one additional XX Sxr′ hybridization pattern was observed: the additional pattern in the CB strain was transmitted (via variant XY Sxr carriers) while the secondary XX Sxr′ pattern in the CB′ strain could only be observed once. Thus ‘DNA finger printing’ with oligonucleotide probes can successfully be used to discriminate the DNAs of normal Y chromosomes, XX Sxr and XX Sxr′ variants as well as XY Sxr and XY Sxr′ carrier mice. Implications of the comparatively high unequal recombination rate involving the murine Y chromosome are discussed, as well as possible mechanisms.