The mutations which block lycopene cyclization and those which stop substrate transfer along the carotene pathway are very closely linked in Phycomyces. Simultaneous blocking of both processes commonly results from single exposures to mutagens; and both blockings may be simultaneously removed after a second exposure. The frequencies of different kinds of mutants after treatments with the mutagens N-methyl-N′-nitro-N-nitrosoguanidine and ICR-170, their reversion patterns, and recombination analyses indicate that lycopene cyclization and substrate transfer are governed by separate segments of a single bifunctional gene.

In eukaryotic chromosomes, large blocks of satellite DNA are associated with regions of reduced meiotic recombination. No function of highly repeated, tandemly arranged DNA sequences has been identified so far at the cellular level, though the structural properties of satellite DNA are relatively well known. In studying the joint action of meiotic recombination, genetic drift and natural selection on the copy number of a family of highly repeated DNA (HRDNA), this paper looks at the structure–function debate for satellite DNA from the standpoint of molecular population genetics. It is shown that (i) HRDNA accumulates most probably in regions of near zero crossing over (heterochromatin), and that (ii), due to random genetic drift the effect of unequal crossover on copy numbers is stronger, the smaller the population size. As a consequence, highly repeated sequences are likely to persist longest (over evolutionary times) in small populations. The results are based on a fairly general class of models of unequal crossing over and natural selection which have been treated both analytically and by computer simulation.

The electrophoretic expression of the X-linked enzyme glucose-6-phosphate dehydrogenase was examined in heterozygous Macropus robustus embryos and their extra-embryonic membranes. The amnion and allantois, like the somatic tissues of the embryo proper, showed paternal X inactivation while the avascular and vascular yolk sac cells showed evidence of activity of both maternal and paternal alleles.

Two new types of mutants of the FP2 sex factor have been isolated in males of P. aeruginosa strain PAT. Males harbouring FPd mutants are unable to mediate either sex factor or host chromosome transfer, although they retain the exclusion and precipitation characteristics of wild-type males. Males harbouring the FPs mutant apparently have an altered cell surface as indicated by their loss of precipitability, and although their donor properties are similar to those of wild-type males they show a slightly reduced conjugal fertility.

A previously described sex factor mutant FP* (Stanisich & Holloway, 1972) can be transferred to males carrying either the FPs or FPd factors, and the heterozygous strains produced show restoration of wild-type properties, i.e. wild-type precipitation characteristics of the FPs mutants, and transferability of FPd mutants respectively. This suggests that the mutations of the FPs and FPd factors are recessive to the alleles carried by the FP* factor. The ability to produce such heterozygous strains supports the view that at least two copies of the FP2 factor occur in strain PAT males.

This paper describes a method for selecting for conditional lethal mutations in the filamentous fungus Schizophyllum commune. The method is, to our knowledge, the only successful application of filtration enrichment to Basidiomycetes. In addition, it is far more powerful than filtration enrichment methods reported previously for any fungus; it permits recovery of up to 80% auxotrophs starting with material untreated with any mutagen.

Divergent selection for abdominal bristle number was carried out for 47 generations, starting from a completely homozygous population of Drosophila melanogaster. All lines were selected with the same proportion (20%) but at two different numbers of selected parents of each sex (5 or 25). A significant response to selection was obtained in 25 lines (out of 40). In most cases, it could be wholly attributed to a single mutation of relatively large effect (> 0·3 phenotypic standard deviations). A total number of 30 mutations were detected. In agreement with theory, larger responses in each direction were achieved by those lines selected at greater effective population sizes. A large fraction of mutations were lethals (10/30). Thus, the observed divergence between lines of the same effective size selected in opposite directions was smaller than expected under neutrality. The ratio of new mutational variance to environmental variance was estimated to be(0·52±0·09)×10−3.

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.

Genetic exclusion is the ability of a primary infecting phage to prevent a secondary infecting phage from contributing its genetic information to the progeny. The molecular mechanism of the phenomenon is not well understood. The two genes in phage T4 mainly responsible for genetic exclusion are the immunity (imm) gene and the spackle (sp) gene. Evidence is presented that the imm gp enables the host exonuclease V to degrade superinfecting phage DNA. This appears to be accomplished by the imm gp altering gp 2/64, the presumed pilot protein, which protects the 5′ end(s) of the phage DNA. Exonuclease III is also involved in genetic exclusion but its action does not appear to depend upon the imm or sp gene products. Gp sp appears to interfere with the lysozyme activity of gp 5, a component of the central base plug, postulated to aid in tail tube penetration during the injection process. A molecular model of genetic exclusion is proposed. Genes imm and sp are part of a cluster of genes which also includes 42, beta-glucosyltransferase, and uvsX. The genes of this cluster encode proteins apparently adapted for competition and defence at the DNA level. These genes may encode fundamental adaptive strategies found throughout nature.

We present data on the effects of three chromosome 17 deletions on transmission ratio distortion (TRD) and sterility of several t-haplotypes. All three deletions have similar effects on male TRD: that is, Tdel/tcomplete genotypes all transmit their t–haplotype in very high proportion. However, each deletion has different effects on sterility of heterozygous males, with Tor/t being fertile, Thp/t less fertile, and Torl/t still less fertile. These data suggest that wild-type genes on chromosomes homologous to f-haplotypes can be important regulators of both TRD and fertility in males, and that the wild-type genes concerned with TRD and fertility are at least to some extent different. The data also provide a rough map of the positions of these genes.

We develop a model to predict the increase in genetic variance of a quantitative character in a hybrid population produced by crossing two previously isolated populations of the same species. The increase in variance in the F2 hybrids, the ‘segregation variance’, is caused by differences in the average allelic effects at each locus and by linkage disequilibrium among loci. We focus on the case in which the character is additively based and the average value of the character does not differ in the two populations. In that case the predicted segregation variance depends strongly on what is assumed about the genetic basis of the character. If the genetic variance of the character in each population is attributable to loci with numerous alleles of small effect that are in moderate frequency, as in Lande's (1975) model, the segregation variance should increase linearly with time since the populations were isolated, at a rate determined by the inverse of the effective population size. If the genetic variance is attributable to loci with alleles in very low frequency, as in Turelli's (1984) house-of-cards model or in Barton's (1990) model of pleiotropic, deleterious alleles, then the segregation variance in the hybrid population increases at a much lower rate.

Genetic analysis of seven dominant short tailed mutations independently induced by radiation of male mice showed that six were allelic to T (Brachyury) but not identical to it. Homozygotes for each mutant die at least 2 days earlier than T/T homozygotes; two that were studied histologically are indistinguishable from one another. The development of these abnormal embryos is arrested by seven days of gestation, when cells of embryonic ectoderm cease proliferation and become pycnotic. Endoderm and extra-embryonic ectoderm do not seem to be primarily affected, and survive and grow for at least 2 days more. Serological studies of one of these mutations suggest that it is a deletion. A review is presented of these and other T-like mutations that have been described; from this it appears that five different categories of T-like mutants are discernible.