1. Two total and five leaky sorbitol mutants isolated in Aspergillus nidulans by defective growth on the sugar are all recessive. The mutants are closely linked, they appear to represent three linked genes spanned by a deletion.

2. Mutants which complement in heterozygous diploids do not complement in balanced heterokaryons. Failure to complement is a property of the mutants and not the result of a nutritional interaction or an unfavourable nuclear ratio in the heterokaryons.

3. Sorbitol is oxidized by an inducible enzyme system in the wild-type. There are at least two enzymes concerned in the oxidative assimilation of sorbitol, an initial oxidative enzyme, which is defective in the leaky mutants, and a later enzyme defective in the total mutants. There may also be a second non-oxidative pathway for sorbitol metabolism.

4. In diploids complementary pairs of mutants oxidized sorbitol at 75% the rate of the wild-type but non-complementary mutants did not oxidize the sugar. In balanced heterokaryons none of the pairs of mutants oxidized the substrate. It is concluded that failure of inter-genic complementation in the heterokaryons is the result of a failure of either enzyme formation or enzyme function. Models to account for differences in enzyme formation in heterokaryons and diploids are suggested.

Under a two-locus model with additive genes which combine multiplicatively to determine a quantitative trait, heterosis is generally observed in the F1 It is positive only if both frequencies of the best allele at each locus are not higher in the same parental population. In the F2, heterosis depends on the rate of recombination between the two loci. If linkage is tight, F1 superiority is nearly halved in the F2. But if the two genes are independent, heterosis is maintained in the F2 at the same level as in the F1.

This paper describes the aspects of fertility that had been affected by selection on litter size. For twelve generations previously the mice used as parents were chosen because they had been born in large or small litters. At the end of this time, litters in the fertile strain averaged 11·1 young born alive, while the less fertile strain averaged 5·5.

It was found that male fertility and inherent viability of the young had nothing to do with the response although neither was excluded by the method of selection. Several contributions, however, were made by the females, who were affected not only in ovulation rate, but also in their control of pre-implantational losses, foetal mortality and mortality of the newly born.

Females from the less fertile strain were particularly prone to pre-implantational loss of eggs. It remains to be shown whether these were due to fertilizational or implantational failure.

The incidence of earlier and later embroyonic losses in females of the same strain were uncorrelated—Utters that were depleted early were neither more nor less inclined to be depleted later.

A male mouse with irregular white spotting, typical of piebald, s, arose during an experiment designed to search for mutations induced in spermatogonial cells by ethylnitrosourea (ENU). On being examined cytologically it was found to carry 40 chromosomes but was effectively XXY since one of the two X chromosomes present was distally fused to a Y chromosome. In common with the previously described XXY mice, all of which carried 41 chromosomes, the mouse was sterile with a total absence of germ cells. Because of this, it was not possible to determine if the white spotting was inherited. The spotting could not be related to any observable abnormality of chromosomes known to carry spotting genes, nor could it be linked in any way with the X and Y fusion. It was concluded from the cytological considerations and the time interval (6 months) that had elapsed between mutagen treatment and birth of the offspring, that whereas the spotting was probably the result of ENU damage in a spermatogonial stem cell, the XY fusion was probably a later and spontaneous event.

A sex-linked recessive gene with visible effect will first be detected in the hemizygous sex (male). In lines with equal numbers of males and females, when the gene is initially present in a single female the probabifity of detection falls from 2/3 in single pair lines to 0·54 in large lines. The mean and standard deviation of time to detection are almost independent of population size, being about 4/3 and 2/3 respectively. About 98% of all detections occur within three generations, so a gene detected much later than this after the foundation of a selection line is likely to be a new mutant. Higher initial frequencies and selection favouring heterozygotes increase the chance of detection. The time taken is decreased with higher initial frequencies and increased slightly by selection favouring heterozygotes.

A new allele at the W-locus ( W19H), found in a mutagenesis experiment in which females were irradiated, involves a presumed deletion. The deletion covers the Ph locus (which forms part of a gene complex with the W, Ph and Rw loci), and the locus of a recessive lethal 2 cM distal to W. It does not extend distally to the bl locus; nor does it involve the Rw locus, W19H/Rw compounds being viable and fertile. Thus, the length of the deletion is 2–7 cM. The non-involvement of Rw shows that, in the gene triplet Rw, W, Ph, Rw must lie proximal to W and Ph, whose relative position remains unknown. Heteozygotes for W19H are not anaemic, show only minimal white spotting and no pigment dilution; they thus resemble heterozygotes for the original W mutant allele and differ from W/Ph trans heterozygotes, which have extensive white spotting. In addition W19H heterozygotes may be small and runted, many are believed to die prenatally, and some in the nest. Their radiosensitivity is increased. Homozygotes die at the pre-implantation stage.

A strain of Drosophila, homozygous for the variably penetrant gene tu bw, which causes the formation of abnormal masses of melanizing haemocytes (melanotic tumours), has been reared on defined axenic diets containing various sterols, both singly and in pairs. Both optimal and deficient nutritional levels of sterol have been employed, as well as certain sterols inadequate by themselves to support development. The effect of these diets upon probability of tumour formation has been studied in relation to their nutritional adequacy, as defined by the growth-rate, survival, and in one case, adult body-weight.

The results demonstrate a rather complex pattern of interaction between dietary sterols in determining the variables of the phenotype produced, under circumstances suggesting that all the sterols investigated have entered the developing larvae. There is only a partial overall correlation, and occasionally an inverse relationship, between tumour suppressant and growth-promoting properties of particular sterols. Within single molecules, structural sterol features tend to exert their characteristic effects additively upon the phenotype, except for an inadequacy in utilization of molecules containing the Δ7 double bond, which dominates at low concentrations. With pairs of dietary sterols, however, non-additive or ‘saving’ effects are sometimes seen.

It is suggested that the tu bw allele allows the resolution of several discrete developmental functions for sterols and/or their immediate metabolic products in Drosophila, which cannot synthesize its own sterol. However, the molecular nature of these functions is little understood.

In this report we mapped a new MEL11 gene and summarize our population studies of the α-galactosidase MEL genes of S. cerevisiae. The unique family of structural MEL genes has undergone rapid translocations to the telomeres of most chromosomes in some specific Saccharomyces cerevisiae populations inhabiting olive oil processing waste (alpechin) and animal intestines. A comparative study of MEL genes in wine, pathogenic and alpechin populations of S.cerevisiae was conducted using genetic hybridization analysis, molecular karyotypingand Southern hybridization with the MEL1 probe. Five polymeric genes for the fermentation of melibiose, MEL3, MEL4, MEL6, MEL7, MEL11, were identified in an alpechin strain CBS 3081. The new MEL11 gene was mapped by tetrad analysis to the left telomeric region of chromosome I. In contrast, in wine and pathogenic populations of S. cerevisiae, MEL genes have been apparently eliminated. Their rare Mel+ strains carry only one of the MEL1, MEL2, or MEL8 genes. One clinical strain YJM273 was heterozygotic on the MEL1 gene; its mell0 allele did not have a sequence of the gene.

Four surface exclusion systems have been identified amongst a group of F-like plasmids in E. coli: SfxI(F), SfxII (ColV2 and R538-1fin−), SfxIII (ColVBtrp and R1-19) and SfxIV (R100-1 and R136fin−). None of these systems was expressed in stationary phase cells or, except for ColVBtrp, during fin+ transfer inhibition, showing that the surface exclusion gene(s) is usually co-controlled with the transfer genes.

Recipient cells carrying two plasmids specifying different surface exclusion systems did not always express both of these: the overall pattern suggested that the four systems and/or their sites of action are related. There was no surface exclusion between donor cells carrying two plasmids determining different surface exclusion systems and recipient cells carrying a plasmid determining either one of these. Our hypothesis to explain this and other results is that surface exclusion prevents interaction between the tip of the pilus on the donor cell and a receptor site on the recipient cell surface. Pili (probably mixed) with two types of tips would be present on cells carrying two different plasmids, the one unresponsive to the single surface exclusion system of the recipient cells allowing transfer of both plasmids.

Genes controlling the synthesis of the D group of low-molecular-weight (LMW) subunits of glutenin occur on the short arms of chromosomes 1B and 1 D. Their position on chromosome 1 B, relative to the storage protein loci Glu-B1 (long arm) and Gli-B1 (short arm), was estimated by analysing the backcross-one progeny of two different crosses. To estimate recombination between the D subunit genes and Gli-B1, half grains were analysed by two-dimensional electrophoresis. The Gli-B1 locus contains genes for the B group of LMW glutenin subunits, γ-gliadins and ω-gliadins although only the latter were made use of in this study to distinguish the parental alleles. Additionally, the complementary half grains were analysed by sodium dodecyl sulphate, polyacrylamide-gel electrophoresis to estimate recombination between Gli-B1 and Glu B1, coding for high-molecular-weight (HMW) glutenin subunits. The D subunit genes occur at a new locus, provisionally defined as Glu-B2, which lies in between Glu-B1 and Gli-B1, 17 cM from the former and 22 cM from the latter. On the basis of previous mapping data involving Gli-B1, it was concluded that the D subunit genes occur close to the nucleolar organizing region and probably on the short-arm satellite, like Gli-B1.

A spontaneous mutant of Phytophthora drechsleri, resistant to p-fluorophenyl-alanine and two induced mutants resistant to chloramphenicol have been selected and analysed. The pattern of inheritance of the mutant phenotypes was identical and conformed to that expected in a diploid organism.

Inbreeding experiments in Drosophila, particularly those carried out using the ‘balancer equilibration’ technique, have revealed high levels of inbreeding depression. It has been estimated that non-lethal chromosomes have a fitness of 20% or less in homozygous condition compared to chromosome heterozygotes. Deleterious recessive genes are, in principle, capable of explaining such inbreeding depression. In this paper we have asked quantitatively whether the observed high levels are consistent with what is known about numbers of loci and mutation rates. We find that accepted mutation rates are easily high enough, provided that the deleterious genes are fully recessive. Partial dominance, even to the extent of 10% or less, reverses this conclusion. These calculations have been made assuming the multiplicative model. However the arguments are potentially sensitive to certain types of selective interactions, and a model which proposes quadratic gene interaction allows for higher levels of partial dominance. We also test the effect of taking into account a further constraint. Crow and Mukai have argued from estimates of the persistence of new deleterious mutations affecting viability that heterozygotes have a reduction in fitness of around 1–2% per locus, similar to the estimate for lethal genes. Application of this additional constraint would markedly reduce the range of permissible selection coefficients. However we argue that the selective disadvantages in heterozygotes of most mutations affecting fitness are unlikely to be as high as estimated for mutations affecting viability.

We previously identified a primary sex-determining locus, Tas, on mouse Chr 17 that causes ovarian tissue development in C57BL/6J Thp/ + and Torl/ + individuals if the AKR/J Y chromosome is present. We hypothesized that Tas is located within the region of Chr 17 deleted by Thp and Torl and that C57BL/6J carries a diagnostic Tas allele, based on the observation that ovarian tissue develops in XY mice when Thp is on a C57BL/6J inbred strain background, whereas normal testicular development occurs when Thp is on a C3H/HeSnJ inbred strain background. To test this hypothesis, we mated (C57BL/6J × C3H/HeSnJ)F1 females to C57BL/6J Thp/ + hermaphrodites. As expected, half of the XY Thp /+ offspring developed ovarian and testicular tissue while half developed exclusively testicular tissue. Unexpectedly, the inheritance of selected Chr 17 molecular loci was independent of gonadal development, as half of the male and hermaphroditic offspring inherited C3H/HeSnJ-derived Chr 17 loci and half inherited C57BL/6J-derived Chr 17 loci. We conclude that for ovarian tissue to develop in an XY Thp/ + or XY Tort/ + individual (1) Tas must be present in a hemizygous state, which is accomplished by heterozygosity for the Thp or Tort deletions; (2) the AKR/J-derived Y chromosome must be present; and (3) an additional locus involved in primary sex determination must be present in a homozygous C57BL/6J state. This newly identified gene may be one of the previously defined loci, tda-1 or tda-2.