The linear relationship between fourteen allelic p-aminobenzoic-acid-requiring mutants of Aspergillus nidulans was investigated. The mutants were assigned to twelve different mutational sites within one functional region. No case of intra-cistron complementation was found. The order of sites as determined by the distribution of the outside markers in different crosses between paba alleles is consistent and the recombination fractions between the sites are approximately additive. Crossing-over between alleles is associated with strong localized negative interference. The topography of the pabal region is characterized by a marked concentration of the mutational sites in a small part of the cistron.

This paper examines the hypothesis that the associations between alleles at allozyme loci and gene arrangements, which are observed in many Drosophila populations, result from inversions remaining associated with the alleles contained in the gametes in which they originally occurred. The effects of double crossing over in heterokaryotypes and of selection at loci linked to the allozyme loci, which are themselves assumed to be neutral, are studied theoretically. It is concluded that selection at linked loci is unlikely to have an important effect in retarding the decay of this type of association. The literature on associations between allozymes and gene arrangements is surveyed, and it is concluded that a ‘neutralist’ explanation of this sort cannot be excluded, except possibly in some cases where the allozyme locus is outside the inversion breakpoints and crosses over with measurable frequency in heterokaryotypes.

In a series of Lacerta vivipara samples from southern France's central mountains, the distribution of genotypes at the mannose phosphate isomerase (MPI) locus has only been accountable as due to sex linkage in female heterogamety, provided the W chromosome carries only one of the two observed alleles in the populations sampled. This is in perfect accordance with cytogenetical data. Reasons are presented that seem to limit acceptable hypotheses for the recent origin of this sex-linked polymorphism to three: a founder effect, a point mutation in Z chromosomes after crossover suppression, or hitch-hiking with the translocation involved.

1. Rates of gain and loss of acclimatization to temperature of males from two inbred lines and the hybrids between them were measured by recording their survival times in dry air at a lethal temperature (34°C).

2. All hybrid males lost acclimatization to temperature more quickly than did inbred males. B/K males gained acclimatization to temperature more quickly than any other group, but the K inbred males gained acclimatization more quickly than did either the K/B males or the B males. In all cases acclimatization is gained more quickly than it is lost.

3. The extent of acclimatization to temperature, as measured by the difference in survival times of 15°C. and 25°C. acclimatized flies in a range of lethal temperatures, was not found to be different in inbreds and hybrids.

4. The results suggest that hybrids can produce the enzymes necessary for acclimatization to temperature more rapidly than inbreds and confirms the hypothesis that hybrids are biochemically more versatile than inbreds.

5. The difference between the rates of gain and loss of acclimatization to temperature suggests that the processes involved in the enzyme changes are temperature dependent.

6. The absence of a difference in the extent of acclimatization to temperature indicates that both inbred and hybrid D. subobscura are capable of producing those enzymes necessary for temperature acclimatization.

7. The high values of the temperature coefficients for heat death indicate that this process involves protein (enzyme) denaturation.

8. An ageing effect was observed in inbred flies.

1. The low but regular positive correlation between body-size and the duration of the larval period in populations of D. melanogaster has been studied by selecting for large size or shorter development time on aseptic defined diets deficient in RNA and comparing the results with parallel selection on unrestricted yeast diets or on media in which RNA is not a limiting factor.

2. There is a striking contrast according to the nature of the diet during selection. On unrestricted diets and where RNA is adequate there is little or no evidence of correlation between the two characters, but on low RNA media there is a striking correlation whether selection is for large body size or shorter development time.

3. This contrast is accounted for in terms of particular changes in larval growth which can be divided into a first stage of growth to a critical size in the early 3rd instar and a second stage thereafter. The duration of the first stage can be greatly prolonged by inadequate diet but the duration of the later stage appears to be virtually unaffected by such variation although the amount of growth and hence final body-size, may be drastically reduced. The different diets which lead to presence or absence of correlation have enabled selection either to extend the growing period, so that the critical stage is reached later at a larger larval size, or to accelerate the growth rate in the later stage.

4. Variation in the final stage of growth predominates on unrestricted diets and is responsible for the greater part of the variation in body size in unselected populations. Stabilization of body-size about an intermediate optimum refers especially to growth in this later stage.

5. Lines selected for fast development on low RNA media are especially sensitive to minor nutritional variation. Probably only under rather special conditions is it possible to shorten the duration of the larval period and this is compatible with the importance of development time in fitness generally.

6. There is evidence that the restriction of early growth, in the 2nd instar, reduces the size of the 3rd instar mouth-parts. Such reduction is correlated with changes in adult size probably because smaller mouth-parts restrict food intake.

7. The pattern of larval growth suggests a flexible system which can be adjusted to different ecological conditions since the same body-size can be attained by adjusting the amount of growth effected before or after the critical stage. Differ ences in this respect will involve characteristic differences in reaction to environ mental variation and particular nutritional conditions are likely to influence the way in which adaptive changes are realized.

The ‘maxy’ technique was used for scoring the frequencies of whole body and fractional mutations in the progeny of males of Drosophila melanogaster that had been irradiated with 2000 R, irradiation being followed or preceded by treatment with caffeine or acriflavine. Three 2-day broods were used, and males irradiated without subsidiary chemical treatment were used as controls. Both chemicals whether given as post- or pre-treatment strongly reduced the frequencies of fractional mutants in all broods. The frequency of whole-body mutants was unaffected in the first two broods and suffered a moderate reduction in the third. These results are discussed in relation to the hypothesis that repair processes regulate the development of a primary lesion into either a whole-body or a fractional mutant and that the functioning of the repair enzymes depends on the state of maturity of the male germ cell.

When combinations of inhibitors acting on the subunit B of DNA gyrase were tested in Bac. subtilis strains, the growth-inhibiting effect of novobiocin was specifically antagonized by subinhibitory concentrations of coumermycin A1. An antagonism in the opposite direction was not observed.

Two alternative models are proposed, where the supercoiling decrease caused by novobiocin is antagonized by coumermycin.

This phenomenon seems to be characteristic of the Bac. subtilis species.

One hundred and ninety-eight mice trapped along a south–north transect through the Danish hybrid zone between Mus musculus domesticus and M. m. musculus were typed for mitochondrial DNA (mtDNA), the Y chromosome and ten autosomal loci encoding diagnostic proteins. The southern (domesticus) populations display two mtDNA variants (S1 and S2) and the northern (musculus) have a third mtDNA variant (N) of domesticus origin. Across the hybrid zone defined by ten autosomal loci, there is a steep dine between the southern and northern types of mtDNA. As well as confirming an earlier finding that Danish musculus all have a domesticus mtDNA (Ferris et al. 1983a, & b), our results show that this mtDNA takeover is not the result of a persistent mitochondrial gene flow between the two subspecies. While the coincident dines for the ten autosomal loci and the abrupt dine for the Y chromosome can be explained by selection, it is less likely to be the case for the mtDNA exchanges. We discuss the possible role of sex-linked migration and genetic drift to account for the distribution of the mitochondrial variants.

Maps have been made showing the order of am mutant sites using (a) frequencies of am+ recombinants from crosses between am mutants and (b) the modes of distribution of the am+ recombinants among the two parental and two recombinant classes with respect to the flanking markers inos and sp.

It is possible to arrange the sites in an order such that, in almost all the crosses yielding useful numbers of am+ recombinants, the sp allele originally in coupling with the distal am mutant site occurs in the majority of the recombinants. No such consistent pattern was found with respect to the inos marker. The order obtained by reference to sp agreed with the best order deducible from recombination frequencies.

The data are consistent with the hypothesis that am+ recombinants arise by a process of gene conversion, that there is a gradient of conversion frequencies from the right (inos or distal) end of the gene to the left (sp or proximal) end, and that conversion tends to be associated (though less than 50% of the time) with crossing-over, especially on the distal side.

There is no obvious relationship between the map position of a given am mutant and the properties of the protein product of the mutant gene.

The pattern of response expected from fixation of mutant genes for quantitative traits in finite populations is investigated for a range of distributions of mutant gene effects. The eventual rate depends on the total variance of mutant effects per generation, but the initial rate and the variance of response is higher if the distribution of mutant effects has a large standard deviation or is leptokurtic. The difference between initial and eventual rates of response is greater with large population sizes.

For a range of assumptions, new mutants are unlikely to have much influence on response for 20 or so generations, but then may contribute substantially, such that no plateaux are obtained. However, information on the variance contributed by mutants is almost entirely on bristle number in Drosophila.

It is argued that the role of new mutants should be considered in designing breeding programmes, in particular in utilizing large populations.

The Sxr (sex-reversed) region that carries a copy of the mouse Y chromosomal testis-determining gene can be attached to the distal end of either the Y or the X chromosome. During male meiosis, Sxr recombined freely between the X and Y chromosomes, with an estimated recombination frequency not significantly different from 50% in either direction. During female meiosis, Sxr recombined freely between the X chromosome to which it was attached and an X-autosome translocation. A male mouse carrying the original Sxra region on its Y chromosome, and the shorter Sxrb variant on the X, also showed 50% recombination between the sex chromosomes. Evidence of unequal crossing-over between the two Sxr regions was obtained: using five markers deleted from Sxrb, 3 variant Sxr regions were detected in 159 progeny (1·9%). Four other variants (one from the original cross and three from later generations) were presumed to have been derived from illegitimate pairing and crossing-over between Sxrb and the homologous region on the short arm of the Y chromosome. The generation of new variants throws light on the arrangement of gene loci and other markers within the short arm of the mouse Y chromosome.

Linkage data relative to the markers tabby and glucose-6-phosphate dehydrogenase are presented to locate X-linked cataract (Xcat) in the distal portion of the mouse X-chromosome between jimpy and hypophosphatemia. The human X-linked cataract-dental syndrome, Nance–Horan Syndrome, also maps closely to human hypophosphatemia and would suggest homology between mouse Xcat and human Nance-Horan Syndrome genes. In hemizygous males and homozygous females penetrance is complete with only slight variation in the degree of expression. Phenotypic expression in Xcat heterozygous females ranges from totally clear to totally opaque lenses. The phenotypic expression between the two lenses of a heterozygous individual could also vary between totally clear and totally opaque lenses. However, a correlation in the degree of expression between the eyes of an individual was observed. A variegated pattern of lens opacity was evident in female heterozygotes. Based on these observations, the site of gene action for the Xcat locus is suggested to be endogenous to the lens cells and the precursor cell population of the lens is concluded to be small. The identification of an X-linked cataract locus is an important contribution to the estimate of the number of mutable loci resulting in cataract, an estimate required so that dominant cataract mutagenesis results may be expressed on a per locus basis. The Xcat mutation may be a useful marker for a distal region of the mouse X-chromosome which is relatively sparsely marked and the X-linked cataract mutation may be employed in gene expression and lens development studies.