Detectable allelic variation at the Gpi-1 loci on the short arms of the homoeologous group 1 chromsomes in wheat is not common. However, a variant null allele at the Gpi-D1 locus is present in some stocks of Chinese Spring. This has allowed the locus to be mapped between the ω-gliadin locus carried distally on the short arm of chromosome 1D, Gli-D1 (34·5%) and the high-molecular-weight glutenin subunit locus carried near the centromere on the long arm, Glu-D1 (36·2%). The origin of this isoenzyme polymorphism in Chinese Spring stocks is described and its potential significance is discussed in relation to quantitative analysis of aneuploids, alien chromosome addition and substitution lines and intervarietal chromosome substitution lines involving Chinese Spring.

Perculiarities of preimplantation and early postimplantation development were studied in embryos with partial deletions and duplications of chromosomes 7, 9, 14 and 17, in the progeny of mice heterozygous for the unequal reciprocal translocations T(7; 14)2Iem, T(16; 17)43H and T(9; 17)138Ca. Deficiencies for any part of autosomes 9 or 14 combined with duplications of the corresponding segments of autosomes 7 or 17 do not affect preimplantation development, though they are lethal soon after implantation. Deficiency for the distal part of chromosome 7 (Df7F4) induces embryonic death by the early blastocyst stage. Deficiencies for the distal part of chromosome 17 (Df17El–E5), as well as for its proximal region (Df17AB) carrying all genes of the T-t complex, have no detrimental effects on cleavage, blastulation and implantation, but are lethal after implantation, mostly during early neurulation. Deficiency for the middle part of chromosome 17 (Df17CD) is expressed just after a few cleavage divisions, and these embryos all die by the morula stage. It is suggested that the genes of the CD region of chromosome 17 and of the F4 region of chromosome 7 are of major significance for genetic control of early development in the laboratory mouse.

Genetic variation at 11 enzyme loci in Aedes aegypti populations collected from 63 localities around the world is presented. A UPGMA tree based on genetic distance values clusters populations of sylvan A. aegypti formosus from West Africa and East Africa together, along with Asian and south-eastern U.S. populations. Domestic A. aegypti aegypti from East Africa and all other New World populations form the other major cluster. Multivariate discriminant analysis allows recognition of seven major global ‘genetic–geographic’ groups, which are consistent with the genetic distance data. Populations from the south-eastern U.S. are clearly genetically distinct from other U.S. and Mexican populations. This distinct gene pool may be indicative of reinfestation of areas where A. aegypti appears to have been absent in the recent past. Other evolutionary and epidemiological implications of the genetic population structure of Aedes aegypti are discussed.

The degree of heterozygosity as determined by electrophoretic analysis of three or four polymorphic loci correlates positively with survival in age groups of the American oyster (Crassostrea virginica) collected as spat from two different natural populations. The phenomenon is shown to operate in ages from 2 weeks (post-settlement) to 3 years and appears to be general in populations of marine molluscs. The most likely explanation for this result is that heterozygosity improves survival through its effect on growth (heterozygotes grow faster). The effects of individual loci on viability are independent of each other. A direct involvement of the enzyme polymorphisms is the most probable genetic interpretation of the data, but associative overdominance cannot be excluded.

Isolation and characterization of five new nuclease (nuc) deficient mutants of Neurospora have been described. The new mutants are unable to utilize nucleic acids as the sole phosphorus source and possess growth characteristics similar to those nuc (nuc-1 and nuc-2) mutants described previously. Two new mutants (nuc-4 and nuc-5) were able to use RNA or predigested DNA (but not intact DNA) as phosphorus source and showed temperature sensitive growth at 37 °C. Based on the data from complementation and genetic analyses the five new nuc mutants (nuc-3, nuc-4, nuc-5, nuc-6 and nuc-7) were found nonallelic to each other and to previously described nuc (nuc-1 and nuc-2) mutants; the new nuc mutants mapped to the right of arg-12 on linkage group II. On biochemical analyses, these nuc mutants were found to possess a lower level of extracellular nucleases and alkaline phosphatase as compared to the wild type strain. The ds DNase activity of the new mutants was only about 2–12% of that of the wild type strain; thus, the low level of these extracellular enzymes in the nuc mutants causes their inability to utilize nucleic acids as the sole phosphorus source. Wild type levels of these enzymes were restored in the complementing heterokaryons capable of full growth on the DNA medium. Data from intercrosses, mutagen sensitivity and spontaneous mutation-frequency studies (as discussed in a subsequent paper) indicated the involvement of the nuc genes in DNA repair and recombination.

Five new nuc mutants of Neurospora crassa were characterized for their relative sensitivities to different mutagens (UV, MNG, MMS), to mitomycin-C and to histidine; latter has been shown to inhibit the growth of certain UV sensitive mutants. These mutants were also compared for their capabilities for spontaneous mutation as determined by resistance to p-fluoro-phenylalanine. Based on these characterization, the mutants seem to belong to two groups. The first group included nuc-3 and nuc-6 which showed sensitivity to all mutagen tested and possessed capability for a very high frequency of spontaneous mutation (i.e. mutator effect). The second group included nuc-4, nuc-5 and nuc-7; these were as resistant to different mutagens as the wild type strain, but possessed an antimutator effect (i.e. the frequency of spontaneous mutation by these three mutants were at least 0·5–100 × less than the wild type strains). There was some variation in these properties of mutants belonging to the two groups. Among all the five nuc mutants, nuc-3 was characterized by extreme sensitivity to all mutagens. None of the five nuc mutants were sensitive to histidine. The properties of nuc mutants are discussed in relation to their possible role in DNA repair and recombination.

A form of the human skin disease, ichthyosis, results from a mutation at the steroid sulphatase locus (STS) on the X chromosome. This locus appears to escape inactivation in the XX female, resulting in the expression of two doses of the STS gene (Shapiro et al. 1978; Crawfurd, 1982). The scurfy mutation in the mouse is thought to be homologous to the human disease (McKusick, 1978), and so should also be due to a steroid sulphatase (STS) deficiency. Our findings in male and female mice suggest that, in contrast to the human, the murine ‘STS’ locus is subject to X chromosome inactivation. However, another interpretation of the results is possible, namely that STS may be coded for by an autosomal gene.