A map of the seventeen R.SmaI sites within the 33·4 kb transfer region of plasmid F has been obtained. The number of R.SmaI sites contrasts sharply with the few sites for other restriction endonucleases with hexanucleotide specificity. Location of the R.SmaI sites in γtra transducing phages allowed physical location of lambda insertions into the traB, traF and traH genes.

A mutant with the properties of a recipient has been isolated from the P. aeruginosa donor strain PAT (FP 2 + ) following treatment with the acridine-mustard ICR-191. While this strain displays the properties expected of a female or recipient in a number of genetic tests, the FP 2 determined property of mercury resistance is retained by the strain, suggesting that it may carry the FP2 factor in a mutated form. Treatment of the donor strain PAT (FP2 + ) with acridine-mustard has produced mutant male strains with the ability to form recombinants with other male strains at frequencies similar to that obtained in FP2+ × FP2 − matings. This characteristic has been shown to be due to a mutation in the FP2 factor which is dominant to the wild-type function. The isolation of stable male strains carrying both the mutant and wild type forms of the sex factor suggests that more than one copy of the FP 2 factor occurs in P. aeruginosa strain PAT donors.

An electrophoretically detectable variant of acid α-glucosidase has been found in SM/J mice. This variant is attributable to excess sialylation of the enzyme and is determined by a gene, alpha-glucosidase processing, Aglp, on chromosome 17. In addition, as also reported by Potier, Lu Shun Yan & Womack (1979), SM/J mice are relatively deficient in neuraminidase and it appears that the low level of this enzyme in SM/J is determined by an autosomal codominant gene, neuraminidase-1, Neu-1. Preliminary data indicate that Neu-1 is also on chromosome 17. It seems probable that the several processing genes Apl, Aglp and Map-2 which are all closely linked on chromosome 17 are one and the same, a gene Neu-1 coding for neuraminidase.

Mutants of Ustilago maydis have been isolated both, deficient and derepressed for nitrate reduction. Those deficient in enzyme fall into six groups, one of which is the structural gene. Enzyme which has proved to be more labile than that of wild-type has been isolated from a temperature-sensitive mutant at this locus. All the mutants in the structural gene have xanthine dehydrogenase activity and the situation closely parallels that of Aspergillus nidulans.

The derepressed mutants fall into four complementation groups and all are partially derepressed in that they are further inducible by nitrate. Full derepression can be conferred by induction of a second mutation. In one analysed case the second reinforcing mutation proved to be pheno-typically similar to the first one when separated from it.

Results of crosses of a large number of Neurosporas of different origin, including several distinct strains of N. sitophila, were utilized to re-examine the question of whether certain wild-type Neurosporas other than N. crassa show biases in the two types of second-division segregation. Segregations for alleles of the mating type and peak loci on a wide variety of genetic backgrounds gave little evidence for excess either of symmetrical or asymmetrical ‘post-reduction’ asci.

The incidence of many minor skeletal variants in the inbred mouse strain C57BL can be influenced by the diet on which the parents live: in many cases, the effect is mediated by a correlation with body size. This also seems to be true in Falconer's (1973) Q-strain in which body size has been increased or decreased by selection. However, there was so much heterogeneity between replicates within selection lines that variants influenced by body size could be detected as a group, but not identified individually.

This is a study of the chromosomal segregation patterns in females of 15 Experimental stocks of Drosophila melanogaster, each carrying one element of a T (Y; 2) with a centric break-point. In each Experimental stock the relative frequency of all eight possible meiotic configurations of four relevant chromosomal elements was followed: an attached-X chromosome, a multiply-inverted chromosome 2, a free arm of chromosome 2, and a half-translocation element. Although the 15 translocation elements were broken at different sites, there were no basic differences among the Experimental stocks in their segregation patterns. The three two-by-two configurations were the most common. Comparison of this pattern with that of the segregation pattern of stocks similar but for an inversion-free chromosome 2, showed that in the Experimental stocks exchange pairing did not play a significant role in the determination of the segregation pattern.

The results of these experiments, together with the analysis of results from other published studies provide evidence against the model that had been forwarded by Grell. According to this model, chromosomes that did not participate in exchange pairing undergo another pairing cycle, in which total chromosome length is a factor in the determination of segregation.

We support a modified version of Novitski's model of premetaphase chromocenter-like chromosome aggregation. Disjunction of non-exchange chromosomes is regulated by determinants located in the proximal heterochromatin of the sex chromosomes and the autosomes. However, the specificity, especially that of the autosomal determinants, is not high. Thus, if an autosome and a sex chromosome are available, their determinants may interact-to-disjoin by default. More frequently, the determinants of the left-arm autosomal element may interact-to-disjoin with those of the right-arm chromosomal element.

The average effect and average excess both measure the phenotypic effects of gametes in a population. A matrix notation is introduced that provides a general analytical solution for the average effects at a single locus with k alleles that can be solved for any population regardless of its genotype frequencies. This same notation also provides an easy way of deriving and generalizing to k alleles the well-known relationships between average effects and average excesses that exist under random-mating and regular deviations from Hardy–Weinberg equilibrium due to inbreeding.

Mutation-selection balance in a multi-locus system is investigated theoretically, using a modification of Bulmer's infinitesimal model of selection on a normally-distributed quantitative character, taking the number of mutations per individual (n) to represent the character value. The logarithm of the fitness of an individual with n mutations is assumed to be a quadratic, decreasing function of n. The equilibrium properties of infinitely large asexual populations, random-mating populations lacking genetic recombination, and random-mating populations with arbitrary recombination frequencies are investigated. With ‘synergistic’ epistasis on the scale of log fitness, such that log fitness declines more steeply as n increases, it is shown that equilibrium mean fitness is least for asexual populations. In sexual populations, mean fitness increases with the number of chromosomes and with the map length per chromosome. With ‘diminishing returns’ epistasis, such that log fitness declines less steeply as n increases, mean fitness behaves in the opposite way. Selection on asexual variants and genes affecting the rate of genetic recombination in random-mating populations was also studied. With synergistic epistasis, zero recombination always appears to be disfavoured, but free recombination is disfavoured when the mutation rate per genome is sufficiently small, leading to evolutionary stability of maps of intermediate length. With synergistic epistasis, an asexual mutant is unlikely to invade a sexual population if the mutation rate per diploid genome greatly exceeds unity. Recombination is selectively disadvantageous when there is diminishing returns epistasis. These results are compared with the results of previous theoretical studies of this problem, and with experimental data.

Minute (M) lesions exhibit a striking propensity for interacting with many different mutations. In the past, few attempts have been made to explain these diverse phenomena. This study describes a variety of temperature-sensitive (ts) interactions exhibited by the ts third chromosome Minute mutation M(3)LS4Q-III (Q-III). Most of these interactions (i.e. those involving vg, cp, Dl, Dfd or Ly) reflect Q-III-induced enhancement of the respective mutant phenotypes at the restrictive temperature. However, Q-III also suppresses the extra-sex-comb phenotypes of Pc and Msc at 29 °C and evokes lethal and bristle traits when combined with J34e at the restrictive temperature. All of these interactions are characteristic of non-ts Minute lesions and thus they appear to be correlated with general physiological perturbations associated with the M syndrome. In addition, our findings show that mutations that affect ribosome production and/or function, namely su(f)ts67g and bbts−1, exhibit interactions comparable to those elicited by Q-III. Hence, in accordance with previous findings, we argue that most of the Q-III interactions can be attributed to reduced translational capacity at the restrictive temperature. Finally, reciprocal temperature shift studies were used to delineate TSPs for interactions between Q-III and vg (mid to late second instar), cp (about mid-third instar), Dfd (early third instar) and Dl (late second to mid third instar). We believe that these TSPs represent developmental intervals during which the respective gene products are utilized.

The alcohol dehydrogenase (Adh) gene of Drosophila melanogaster is well suited to be a gene expression reporter system. Adh produces a measurable phenotype at both the enzyme and mRNA levels. We recovered a spontaneous transposable element (TE) insertion mutation near the Adh gene. The insertion is a truncated retroposable element, jockey, inserted upstream of the adult Adh enhancer region. Comparisons between the Adhjockey allele and its direct wild-type ancestral allele were made in an isogenic background (i.e. identical cis and trans factors). Differences in Adhjockey expression compared with the wild-type can be attributed solely to the presence of the jockey element. This jockey insertion results in a decrease in adult mRNA transcript levels in the Adhjockey homozygous lines relative to the wild-type counterpart and accounts for a correlated decrease in alcohol dehydrogenase (ADH) enzyme activity. The larval ADH activity levels are not detectably different.

One means of examining the evolutionary significance of molecular variation on the Y chromosome is to identify phenotypes specifically affected by Y-linked genes, and to quantify the phenotypic variation and its correlation to the molecular variation. The functional importance of the Y-linked array of rRNA genes is demonstrated by the ability of Y chromosome to rescue X-linked bobbed lethal alleles, whose lethality is seen in homozygous females. Because low numbers of X-linked rDNA gene copies result in increased developmental time and shortened bristles, and because there is considerable natural variation in Y-linked copy number, a careful examination of Y-linked variation in these two traits may uncover a mode of selection acting on the multigene family. In this study, 36 Y-chromosome replacement lines were tested to detect subtle variation in bristle phenotypes and developmental rates. Correlations among these traits, rDNA gene copy number, and intergenic sequence length were quantified. The absence of significant correlations between phenotypic characters and rDNA copy number or intergenic sequence length suggests that the extant molecular variation in Y-linked rDNA can have at most very small selective effects.

A derivative line of the homothallic Colonia strain of Physarum polycephalum has been isolated which produces plasmodia with high efficiency within clones of amoebae. Using the synergistic effect of ultraviolet light and caffeine, mutants of this line have been isolated which fail to undergo the developmental transition between haploid amoebae and diploid plasmodia (apt mutants). They are isolated by selecting for amoebae which fail to produce plasmodia within clones. Complementation tests of four mutants have shown that they are mutants of four different loci and they are recessive to wild-type. A further analysis of one mutant reveals that the apt-1 locus is unlinked to three other known markers. Crosses of this mutant with heterothallic strains yield progeny which are homothallic indicating that the lesion is not a revertant from a homothallic to a heterothallic mating-type. The use of this system in isolating developmental mutants is discussed.

The probability distribution of the heterogenic (non-identical by descent) fraction of the genome in a finite monoecious random mating population has been derived. It was assumed that in any generation the length of both heterogenic and homogenic segments are exponentially distributed. An explicit expression is given for the expected number of ‘external junctions’ (sites that mark the end of a heterogenic segment) per unit map length in any generation. The latter necessitates the introduction of two higher-order identity relations between three genes, and their recurrence relations. Theoretical results were compared with the outcome of a series of simulation runs (showing a very good fit), as well as with the results predicted by Fisher's ‘theory of junctions’. In contrast to Fisher's approach, which only applies when the average heterogeneity is relatively small, the present model applies to any generation.

Spatial and temporal differentiation in Gerris lacustris and G. odontogaster (Heteroptera, Gerridae) were studied in restricted areas, where one population of each species was subdivided into several subpopulations. The aim of the study was to relate genetic population parameters to ecological population structure studied by mark-recapture methods in the same pond systems. Marked differentiation between the subpopulations and significant enzyme allele frequency changes between subsequent generations were found at several loci. It is suggested that non-selective forces are a sufficient explanation for the observed differences.

Heterozygotes for the reciprocal translocation T(7;15)9H were intercrossed, with albino (c) and underwhite (uw) as genetic markers, in order to study genetic complementation in mouse chromosome 7. Chromosome 15 is known to show normal complementation. Neither reciprocal cross in which one parent was c/c and the other wild type yielded albino progeny at birth although about 17% would be expected, but albino foetuses were recovered when the mother was c/c and father wild type. These products of maternal duplication/paternal deficiency for distal 7 were markedly retarded with small placentae. No albino foetuses were found when the father was c/c and mother wild type, which suggested earlier lethality. Equivalent crosses with uw (chromosome 15) as proximal marker gave normal underwhite progeny when the mother was uw/uw but small placentae, retardation and neonatal death of presumptive underwhites in the reciprocal cross. These abnormal newborn would have had a maternal duplication/paternal deficiency for proximal 7. These and other findings indicate that one region of defective complementation probably lies distal to the breakpoint of T(7;18)50H at 7E2-F2, while another is between the centromere and 7B3. Examination of man-mouse homologies suggests that the loci for three pathological human conditions (Beckwith-Weidemann syndrome, dystrophia myotonia and rhabdomyosarcoma) with differential parental transmission may be located in homologous regions to those affected by imprinting phenomena on mouse chromosome 7.

Glucose-6-phosphate dehydrogenase (G6PD) activity was measured in blood from heterozygotes for the normal allele G6pda and the low activity allele G6pda-m l Neu. In adult mice lower activity was found in G6pda/G6pda-m l Neu than in the reciprocal heterozygote G6pda-m l Neu/G6pda (the maternal allele being listed first). Thus, either the paternally derived allele was over-expressed or the maternally derived allele was under-expressed. By contrast, in younger mice the difference in G6PD activity in reciprocal crosses was less marked. The findings are interpreted in terms of differential imprinting of maternally and paternally inherited information. The explanation offered for age related differences is that, as a consequence of imprinting, either the paternal X-chromosome is preferentially reactivated, or cells in which the paternally derived allele is active are at a selective advantage, and proliferate better than those in which the maternally inherited allele is active.