An autosomal translocation in the tsetse fly Glossina austeni was studied genetically, cytogenetically and for its effects on viability. Flies homo-zygous for the structural change could be identified by outcrossing to wild-type and demonstrating semi-sterility in all the progeny.

A cytogenetical analysis of male meioses in samples of pupae which were sibs of the semi-sterile progeny showed them to be structurally heterozygous for the translocation. Matings of the translocation heterozygotes and homozygotes gave the expected progeny ratios, with the exception of a deficit of females classified as translocation homozygotes. This was due to their sterility or inviability. Those female homozygotes which did breed showed a subnormal lifetime pupal production. These deleterious recessive effects were probably due to the translocation itself although the influence of linked loci could not be ruled out. These effects would prevent the mass rearing of this particular translocation for a tesetse control project.

Two other stocks which showed semi-sterility were found to carry autosomal translocations and two which currently showed holandric inheritance have Y-autosome translocations. One stock with holandric inheritance of extreme sterility carries a double translocation involving two autosomes and the Y chromosome.

Nine methionine mutants of Aspergillus nidulans (six new mutants plus three isolated previously) were examined; five responded to homocysteine, none responded to cystathionine or cysteine.

Ten revertants of one of the mutants, methB3, blocked before homocysteine, were shown to be due to suppressor mutations. The suppressors were divided into six genes on the basis of complementation tests and recombination data. Mutants of two of the genes were semi-dominant in the heterokaryon but recessive in the diploid. Experiments in which conidial ratios in the heterokaryons were determined suggested that semi-dominance of these suppressors is due to a shift in nuclear ratios in the heterokaryon in favour of the suppressor nuclei.

Some of the suppressors were tested for suppression of two other methionine loci; they acted on methG1 blocked before homocysteine, but not on methH2 blocked after homocysteine, although four out of 13 crosses tested gave ambiguous results.

Many inbred and isofemale lines derived from wild populations of Drosophila melanogaster were tested for gonadal dysgenic sterility, male recombination and snw secondary mutation. Among them, we have found strains whose dysgenic offspring show negligible sterility, and undetectable male recombination and snw mutation. They can be considered to be neutral strains in the strict sense. Such neutral strains appear to carry only defective P elements in their genomes. Taking the observations of Karess & Rubin (1984) into account, it is suggested that some defective P elements retain the function necessary for P cytotype. Cytotype determination mechanisms are discussed.

Systematic crosses between various strains of Drosophila melanogaster lead in some cases to partly sterile F1 females (SF females). Two main classes of strain, inducer and reactive, have been denned on the basis of this sterility, which shows very specific physiological features. SF females arise only when reactive females are crossed with inducer males. In contrast, F1 females (RSF) produced by the reciprocal cross between inducer females and reactive males have normal fertility. All wild populations tested are of the inducer category, laboratory strains are either inducer or reactive. Sterility is the result of interaction between two genetic factors denoted I and R, respectively responsible for the inducer and reactive conditions and whose unusual genetic behaviour has been described in other papers. The present paper reports experiments showing that the I–R interaction is also responsible for high levels of X nondisjunction and of mutation in the SF female germ-line. The analogy with the P-M system of Kidwell, Kidwell & Sved (1977b), is discussed as are also the implications of the existence of the I-R system for spontaneous mutation research in D. melanogaster.

A cloned Y-specific sequence (Bishop et al. 1985) was used as a diagnostic probe to distinguish between Mus musculus domesticus and Mus musculus musculusY-chromosomes. Analysis of the RFLPs obtained with genomic DNA isolated from wild mice caught along the contact zone between M. m. domesticus and M. m. musculus in Bulgaria and Denmark showed that the Y-chromosome flow between the two semi-species is very limited. The degree of Y-chromosome penetration was compared with that of seven diagnostic autosomal loci and the mitochondrial DNA. Breeding experiments showed that the lack of Y-chromosome introgression from one semispecies to the other was not due to a major hybrid breakdown. The results suggest that the disruption of differentiated co-adapted gene systems could play a role in limiting Y-introgression.

A chloramphenicol-resistant mutation in Escherichia coli K 12, cmlA1 (previously designated 1a), giving a higher Cm-resistance than other mutations yet examined, has been shown to have a chromosomal location, the gene order being gal, λ, bio, cmlA, pyrD. CmlA can be transduced efficiently into cm-sensitive strains by P1 with little phenotypic lag, and is co-transduced with the λ-attachment site (frequency 1·13%) but not with gal or pyrD.

An electrophoretic variation in a mouse serum protein moving closely to the vitamin D binding protein is described. The variation is determined by two codominant alleles at one locus with the allele in DBA causing fast mobility and that in C57BL causing slow mobility. This locus is located in the proximal part of chromosome 9, 14·3 cM from the d locus and 31·9 cM from the Bgs locus. The protein has not yet been identified but possible candidates among the serum proteins are discussed.

Isofemale lines of Drosophila melanogaster from six localities along the east coast of Australia, spanning 2900 km and 26 degrees of latitude, were assayed for their gonadal dysgenesis characteristics in the P–M system of hybrid dysgenesis. A strong clinal pattern with latitude was discovered. From north to south, the first two populations were typical strong P populations, and the next population was moderate P. The next population to the south was neutral (Q), with some weak P and weak M characteristics. The two southernmost populations were typical M populations. Much variance in P activity in P populations and in susceptibility to P activity in M populations was detected among isofemale lines. This clinal pattern with latitude of the P–M system is paralleled by similar clinal patterns for frequencies of common cosmopolitan inversions and of certain allozymes in Australia. A model of introductions of flies with different characteristics in the north and south could account for the P–M clinal pattern, but cannot account for an intermediate Q population, nor establish the inversion and isoenzyme dines at the same time. Current models of transposable element population dynamics are limited to single population dynamics, and are therefore inadequate for these clinal data.

A cDNA containing the nearly complete coding sequence of CK-III subunit of X. laevis was isolated, sequenced and further identified by comparing the tissue distribution of CK-III/III isozyme with that of its messenger. Comparison of CK-III deduced amino acid sequence with other CK sequences published reveals its close homology to M-CK subunits. Results using both cDNA probes and monoclonal antibodies specific for CK-III subunits indicate that the appearance and the accumulation of CK-III occur in parallel with myoblast differentiation. Moreover, subcellular immuno-histolocalization shows that CK-III/III isozyme is especially concentrated on larval myofibres at the level of A-bands.