A new gene designated sG was identified in Aspergillus nidulans by mutation affecting the enzyme sulphite reductase and leading to a strong derepression of arylsulphatase and enzymes constituting the alternative pathway of cysteine synthesis. The results indicate that proper physiological functioning of this pathway is strongly dependent on full activity of the sulphate assimilation pathway.

The hordein polypeptide controlled by the Hrd G (Hor 4) locus in Elgina and derived lines was purified by preparative isoelectric focusing. The amino acid composition was similar to those of the major B hordeins encoded by the Hor 2 locus. Genetic analysis confirmed that Hor 4 is located proximally to Hor 1 on the short arm of chromosome 5. It is speculated that Hor 4 arose by translocation of genes from Hor 2, possibly in an ancestor of Elgina.

A barley endosperm cDNA clone was used to study the polymorphism and chromosomal location of β-amylase genes in barley. Analysis of DNA from seven cultivars digested with three restriction endonucleases showed two types of pattern, one present in Sultan and the other in the remaining six cultivars. A copy-number reconstruction indicated the presence of about three gene copies per haploid genome. Analysis of the six available whole chromosome addition lines and selected telocentric chromosome additions of barley into wheat showed the location of genes on the short arm of chromosome 2 (probably one copy) and the long arm of chromosome 4 (probably two copies).

XY and XX doublesex D. melanogaster, expressing variable intersexual phenotypes, were compared for their pheromone levels (e.g. 7, 11-heptacosadiene, the main excitatory pheromone of females, and vaccenyl acetate, an inhibitory compound produced only by males). Despite the intersexual phenotype and the presence of female traits, the pheromone patterns of the homozygous dsx mutants, XY as well as XX, were similar to those of heterozygous males. Female-specific dienes were never found in significant amounts in such flies, which often showed significant amounts of the male-specific acetate and triggered very reduced levels of male courtship wing vibration.

The murine mutation, Cat Fraser (CatFr), causes dominantly inherited ocular cataracts. Lenses of adult mice bearing this mutation contain reduced amounts of all seven γ-crystallin proteins and their corresponding transcripts. Levels of other lens proteins and transcripts appear normal and no extra-ocular effects of the mutation have been observed. The selective effect of this mutation on the γ-crystallins is consistent with the possibility that the site at which it occurs is involved in the coordinated regulation of the family of genes which encodes them. We have shown that several restriction fragment length polymorphisms in the γ-crystallin genes segregate independently of the CatFr mutation. Therefore, despite its selective effect on the expression of the γ-crystallin genes, the mutation is not linked to them. This observation rules out the possibility that the mutation is in a cis-acting regulatory site.

Fifty-seven mouse strains were examined for genetic variation at 21 esterase loci. Three new alleles were found: Es-6d in strain A/WySna, Es-lle in FTC/CpbU and Es-18c in two WLL/BrA sublines. At most loci there was a single allele found in over 80% of strains, with one or two rare alleles. However, the Es-1, 3, 10, 13, 25 and 27 loci were much more polymorphic. Although several loci were linked on chomosomes 3, 8 and 9, linkage disequilibrium was only found between Es-5 and Es-11 (chromosome 8) and Es-26 and Es-27 (chromosome 3). There was also significant disequilibrium between Es-1 and 3, Es-1 and 10, and Es-3 and 10, which are on different chromosomes, suggesting that the 57 strains are not a random sample of inbred mouse strains. Fifty-four strains were closely related, with the Es-7b, –17a, –18a, –23c set of alleles, which are typical of Mus musculus domesticus. The three exceptional strains were MOL3 (Mus musculus molossinus), WLL/BrA (English–Norwegian origin) and TA2 (Chinese origin). There were 10 groups of strains which were identical at all loci. Sublines of the same strain were usually identical. Sometimes more distantly related strains, such as CBA/Bi, C3H/He, SM and DBA/Li, were identical, and in a few cases strains with no known common ancestry such as C58 and MAS were identical. Attempts to discriminate between a subset of 22 American and 15 European strains were unsuccessful, suggesting that the European strains add only in a quantitative manner to the gene pool of ‘laboratory mice’, whereas wild-derived strains such as MOL3 are genetically quite distinct from other laboratory mice.

A viable anaemic mouse mutant arose in the stock of a mouse fancier and has been characterized haematologically and genetically. Anaemic animals were less viable than normal animals (especially from 0 to 2 weeks of age) and had lower haemoglobin levels, percentage packed-cell volumes, higher red cell counts and lower mean cell volume than normal animals. Peripheral blood films showed a wide range of abnormal cells and extreme microcytosis. Linkage studies showed the mutant to be linked to the chromosome 15 markers Na Ca and bt; recombination with Ca was 1·37 ± 0·68 % for females and 10·5 ± 7·41 % for males. This position is similar to the microcytic anaemia, mk, mutant, and crosses between the viable anaemia mutation and mk/mk homozygotes showed the two to be allelic. Viable anaemia is therefore a second allele at the mk locus mkvan; new data give its position on chromosome 15.

Variance components of fitness under the stabilizing selection scheme of Wright (1935) for metric characters are calculated, extending his original analysis to the case with any number of alleles and multiple characters assuming additivity of gene effects. They are calculated in terms of the moments of the effects of alleles at individual loci for the metric characters. From these formulas, the variance components of fitness are evaluated at the mutation–selection equilibria predicted by the ‘Gaussian’ approximation (Lande, 1976), which is applicable if the per locus mutation rate is high, and the ‘House of Cards’ approximation (Turelli, 1984), which is applicable if the per locus mutation rate is low. It is found that the additive variance of fitness is small compared to non-additive variance in the ‘Gaussian’ case, whereas the additive variance is larger than non-additive variance in the ‘House of Cards’ case if the number of loci per character and the number of characters affected by each locus are not too large. With the assumption that a significant portion of fitness is due to this type of stabilizing selection, it is suggested that the real parameters are in the range where the ‘House of Cards’ approximation is applicable, since available data on variance components of fitness components in Drosophila show that the additive variance is far larger than the non-additive variance. It is noted that the present method does not discriminate the two approximations if the average values of the metric characters deviate from the optimum values. Other limitations of the present method are also discussed.

The amount of linkage of disequilibrium maintained in a two-locus infinite population model by gene conversion and recombination is examined. Intrachromosomal conversion (conversion between different loci on the same chromosome) generates positive linkage disequilibrium. Specifically, = p(1 − p) [1 − r/(γ + r − γr)], where p is the frequency of allele A at both loci, r is the recombination rate between loci and γ is the per-gamete conversion rate. Somewhat unexpectedly, interchromosomal conversion (conversion between loci on different chromosomes) also generates positive disequilibrium, albeit very small. More interestingly, the behaviour of this disequilibrium as a function of recombination is unusual. If β is the interchromosomal conversion rate between a pair of loci, then = p(1 − p) [rβ/(β+r − βr)]. increases with increasing recombination, being zero for the case of complete linkage (r = 0), and maximized at r = 1/2. This unusual behaviour can be accounted for by the generation of excess coupling gametes when an interchromosomal conversion event is followed by recombination.

A polygenic model has been simulated in order to reveal the process whereby selection in an infinite population can lead to an increase in the frequency of alleles causing higher rates of recombination (CH alleles). Directional selection generates repulsion linkage disequilibrium (+ − + −), which is less strong in CH gametes (gametes carrying CH alleles). In consequence, CH gametes contribute greater phenotypic variability, and therefore respond more to directional selection: that is, they accumulate more selectively favoured alleles. CH alleles then increase in frequency by hitch-hiking. In contrast, normalizing selection, or frequent changes in the direction of selection, favour alleles for a low recombination rate.

The normal response to injection of noradrenaline (NA) in newborn lambs is an increase in metabolic rate and rectal temperature, due to the stimulation of non-shivering thermogenesis. In a previous study 6 out of 7 lambs born to a sire previously selected for low resistance to cold failed to show this characteristic response and were termed non-responders. The sire, 2 of his male offspring and 6 sires selected randomly from the flock were mated to several ewes and the response to NA stimulation recorded in 116 newborn lambs. Control sires produced only normal responder lambs whereas the remaining sires all produced both responder and non-responder lambs. The proportion of non-responders was not significantly different from 0·50, which is consistent with a dominant major gene. Analysis of the quantitative traits, peak metabolic rate and peak rectal temperature following NA injection confirms that a major gene is segregating in the study population, but is unable to distinguish between dominant and recessive modes of inheritance. Absence of non-responders in other studies suggests that dominance is more likely. This new genetic resource could aid our understanding of brown adipose tissue metabolism and the effect of catecholamines on metabolic pathways.

We constructed a cloning vector (pMT603) based on the low copy number plasmid SCP2*. pMT6O3 is unstable because it lacks the SCP2* stability region and carries the selectable marker thiostrepton-resistance and a tyrosinase gene which results in melanin production. This allows easy testing of plasmid stability and we demonstrated its usefulness by cloning a plasmid stability function.