In mice homozygous for the asebia mutation (abJ/abJ) the sebaceous glands were small and the sebaceous cells abnormal, the fully grown hair follicles were twice as long as those in wild-type (+ / +) mice, the catagen and telogen follicles were abnormal and, because the active phase of the hair cycle was longer than in + / + mice, the initiation of the second hair cycle was delayed. The abnormalities in the sebaceous glands and in catagen and telogen follicles were also present in abJ/abJ embryonic skin grown on a nude host but anagen of the second hair cycle commenced at about the same time in abJ / abJ and + / + grafts. When recombinants incorporating mutant or wild-type epidermis and dermis were grown on a nude host, the abnormalities in the sebaceous glands and the catagen and telogen follicles were only observed in the recombinants incorporating abJ / abJ epidermis. It was concluded that mutant activity in the epidermis was responsible for the abnormalities in the sebaceous glands and in catagen and telogen follicles and that mutant activity at some site distant from the skin was responsible for the abnormalities in the timing of the hair cycles.

Genet. Res., Camb. (1986), 47, pp. 93–102

Phosphatase regulation in Aspergillus nidulans: responses to nutritional starvation

By Mark X. Caddick, Alan G. Brownlee and Herbert N. Arst

An error occurred in the heading of Table 3 on page 98. The Table should read as follows:

When DNA sequence data on various kinds of homologous genes sampled from two related species are available, there is a way to infer the effective size of their ancestral species, which is a simple consequence of gene genealogical considerations. This method, when applied to the common ancestral species of human and rat, human and mouse, human and bovine, or rodents and bovine estimates their effective sizes all to be of the order of 107, supporting the view that these species indeed shared, around 75 million years ago, a common ancestral species from which they are descended. The effective size thus estimated would imply that the ancestral species was abundant enough to have ample opportunity for adaptive radiation. The extent of silent polymorphism in that species might have been very large, possibly comparable to the number of silent substitutions accumulated in a gene after the mammalian divergence. Some causes that may alter these results and require a more elaborated statistical analysis are discussed.

By using a simple model of gene conversion, the actual number of alleles contained in a multigene family was theoretically studied. It was shown that the Ewens' sampling theory is applicable to predict the actual number in a gene family of a genome. However, the actual number of the gene family forming the total population becomes larger or smaller than the predicted value by the sampling theory, depending upon the relative magnitude of the rates of two homogenization processes, i.e. intra-genome and in the population.

A cloned Y-specific sequence (Bishop et al. 1985) was used as a diagnostic probe to distinguish between Mus musculus domesticus and Mus musculus musculusY-chromosomes. Analysis of the RFLPs obtained with genomic DNA isolated from wild mice caught along the contact zone between M. m. domesticus and M. m. musculus in Bulgaria and Denmark showed that the Y-chromosome flow between the two semi-species is very limited. The degree of Y-chromosome penetration was compared with that of seven diagnostic autosomal loci and the mitochondrial DNA. Breeding experiments showed that the lack of Y-chromosome introgression from one semispecies to the other was not due to a major hybrid breakdown. The results suggest that the disruption of differentiated co-adapted gene systems could play a role in limiting Y-introgression.

The effects of mutation on mean and variance of response to selection for quantitative traits are investigated. The mutants are assumed to be unlinked, to be additive, and to have their effects symmetrically distributed about zero, with absolute values of effects having a gamma distribution. It is shown that the ratio of expected cumulative response to generation t from mutants, , and expected response over one generation from one generation of mutants, , is a function of t/N, where t is generations and N is effective population size. Similarly, , is a function of t/N, where is the increment in genetic variance from one generation of mutants. The mean and standard deviation of response from mutations relative to that from initial variation in the population, in the first generation, are functions of . Evaluation of these formulae for a range of parameters quantifies the important role that population size can play in response to long-term selection.

The autosomal recessive gene, dysgenetic lens (dyl) in the mouse has been mapped on chromosome 4. Two- and three-point crosses involving b (brown) and Mup-1 (Major urinary protein-1) indicate the following gene order: dyl–b–Mup-1. The approximate distance between dyl and b is 12 and between dyl and Mup-1 is 20 cM.