Twenty t haplotypes were extracted from wild mice captured at several locations in Europe, Israel, North Africa, and South America. The haplotypes were designated tTuw1 through tTuw20. The H-2 haplotypes of the lines were defined using antisera and monoclonal antibodies specific for private antigenic determinants controlled by known H-2 alleles and by antisera produced using the new t lines as donors. The tTuw haplotypes fall into four groups according to the H-2 haplotype associated with them. Haplotypes tTuw10 through tTuw18 are associated with H-2W30, previously found to be linked with haplotypes of the tw1 group. Haplotypes tTuw1 through tTuw6 are associated with a new H-2 haplotype, H-2w36, characterized by the determinant H-2.107. Haplotypes tTuw7 through tTuw9 are associated with another new H-2 haplotype, H-2w37, characterized by determinants H-2.108 and H-2.111. And finally, haplotypes tTuw19 and tTuw20 are associated with yet another new H-2 haplotype, H-2w38, characterized by determinants H-2.33 and H-2.109. These findings suggest that the t polymorphism might be more extensive and more intricate than it was previously thought to be and that at least some of the t-associated H-2 haplotypes, and probably also the t haplotypes themselves, are related to one another in their origin.

We consider an age-structured population that is observed at times t = 0, 1, 2,…. It is assumed that for each t there is the same number of individuals of a particular sex and age group. Another assumption we make is that an offspring of a specified sex has at all times the same probability of having a parent of a particular age and sex. It is shown that the rate of substitution of neutral mutants is /L, where and L are respectively equal to the mean fraction of mutants among gametes succeeding in forming newborn individuals and the mean age of reproduction. This result also applies to monoecious populations. The substitution rate is also derived for advantageous mutants in a monoecious population. Once again, the mutation rate in the usual expression is replaced by /L. Implications of these results are discussed.

Selective differences among male Drosophila melanogaster due to differences in ability to compete for mates may often have been under-estimated in the past because, under the test procedure used, females did not represent a limited resource. In the experiment reported here, no difference was detected between inbred and outbred males ‘competing’ to mate with an equal number of females. When the receptive female: male ratio was halved a large reduction in male mating ability due to inbreeding became apparent.

Two physiologically and biochemically distinct groups of α-amylase (E.C.3.2.1.1) isozymes are synthesized when isolated aleurone layers of barley are incubated with gibberellic acid (GA3). Isoelectric focusing of the α-amylases showed that the isoelectric points of the isozymes of one group were near pH 5, whereas those of the second group were close to pH 6. Using wheat–barley addition lines, the genes for these groups were located in barley chromosomes 1 and 6 respectively. Joint segregation in the F2 generation of appropriate crosses indicated that the isozymes within each group were inherited collectively, and were attributed to codominant alleles segregating at two presumably complex loci, α-Amy 2 and α-Amy 1.

The extent of genetic variation at these two loci was examined in 40 lines of Hordeum spontaneum (the wild progenitor of barley), and in a complex gene pool representative of H. vulgare (composite cross XXI). Variation at the α-Amy 1 locus was much more extensive than that at the α-Amy 2 locus. The genetic variation at both α-amylase loci exceeded that at the majority of other allozyme loci. However the α-amylase loci were less variable than the two loci coding for the seed storage protein, hordein. The wild species was found to contain much genetic diversity, which might be useful in modifying α-amylase activity by breeding. Parallels between the genetics and variation of α-amylase in barley and wheat were noted.

Selection against harmful mutations in large populations is studied assuming that the rate of fitness decrease grows with every new mutation added to a genome. Under this reasonable assumption (Mayr, 1970) the average fitness of a sexual population, without linkage between the loci, is higher, and the average equilibrium number of harmful mutations per individual lower, than in an asexual population. If a gamete contains on the average one or more new mutations, the resulting advantage of sexual reproduction and recombination seems to be sufficient to counterbalance the double advantage of parthenogenesis. Moreover, selection against harmful mutations is probably the most powerful factor preventing linkage disequilibrium even with epistatic interaction between the loci.

Wild-type Friend murine leukaemia (clone 707) cells and two thymidinekinase-deficient subclones, 707BUE and 707BUF, were compared for sensitivity to killing and mutagenesis by the chemical mutagens, ethyl methane sulphonate (EMS), N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), mitomycin C (MMC), and methyl methane sulphonate (MMS). The two thymidine-kinase-deficient subclones were significantly more sensitive to killing by each of the four chemical mutagens than were wild-type cells. The increased sensitivity to killing by the four mutagens was also reflected in increased mutagenesis (per unit dose of mutagen) to 6-thioguanine resistance. In the light of these results, the significance of thymidine kinase in DNA repair and mutagenesis is discussed.

Evidence for close genetic linkage between the structural loci for serum albumin (Alb) and serum vitamin D binding protein (Gc) in chicken is presented. The results are based on a study of a single sire family comprising 36 informative offspring. No recombinants have been observed. It is concluded that this linkage in the chicken is homologous to the close linkage of the albumin and Gc loci reported in man and the horse. Thus, this linkage group has most probably been conserved for at least 300 million years.

The linkage of the locus of the major liver protein, Lvp-1, has been established on chromosome 6. Testcross data show the following gene order and recombination percentages:

centromere −Hd−7·4 ±2·4%−Lvp-1−13·2±3·1% −mi

Data from 39 recombinant inbred strains show complete concordance of the Lvp-1 locus and the Lyt-2 locus on chromosome 6.

The interpretation of gene conversion data from ordered eight-spored asci

By J. R. S. Fincham, W. G. Hill and E. C. R. Reeve

Genetical Research, Vol. 35, No. 2, 1980

On p. 181 the phrases ‘wild to mutant’ and ‘mutant to wild’ in lines 8–9 in the third paragraph should be interchanged: p and r are correction frequencies from mutant to wild and q and s are correction frequencies from wild to mutant, as is apparent in the Table immediately following.

On p. 188 the calculated ratios p/q and r/s may appear to be at variance with the values given in Table 2. This is due to the latter having been rounded to two significant figures. The more accurate values for the + × h3 cross are as follows: p = 0·043, q = 0·161, r = 0·157, s = 0·426 (firstsolution) and p′ = 0·026, q′ = 0·493, r′ = 0·243 and s′ = 0·128 (second solution).

On p. 191 (foot of page) some primes are misplaced. The correct formulae for r, q and s (as given on p. 182) are:

On p. 194, line 7, G = 2B + C should read G = 2B + D.