Thirty-one inbred strains were tested for their reaction to drinking water which contained a low concentration (10−4 M) of sucrose octaacetate (SOA). One strain, SWR, showed a strong aversion to drinking the SOA solution. The other thirty strains, and two samples of wild-derived mice, tended to prefer the SOA solution to untreated drinking water. The pheno-typic difference between SWR and the other strains was shown to be determined by an autosomal gene. The allele present in SWR is dominant. The gene is not closely linked to jerker (je), pearl (pe) or waved-2 (wa-2).

The recovery of two EMS induced mutations which are dominant suppressors of the lethality of cryptocephal in Drosophila melanogaster are described. One of these mutations Su(crc)1 is described in detail. It maps very close to cryptocephal at 54·7 on the second chromosome and its suppression of cryptocephal is temperature-sensitive. Temperature shift experiments show that the temperature-sensitive period is from before the pupariation until 12 h post pupariation. The temperature-sensitive period of Su(crc)1 is discussed in relation to the expression of l(2)crc, head eversion and the timing of pupal chitin synthesis.

I develop a mathematical model which can account for a distribution of the number of repeated genes per chromosome under the joint effects of sister chromatid exchange (SCE), inter-chromosomal crossing-over (ICC), and selection. The model can be applied not only to the cases of small gene clusters but also to multigene families. Based on this model, an appropriate mathematical formula is derived and used to obtain the equilibrium distribution. Assuming stabilizing selection and two simple schemes concerning SCE and ICC, I numerically calculate the equilibrium distribution and compare the result with observations on frequencies of single and triple α-haemoglobin genes in primates. It is also shown that if SCE and ICC occur according to the same probabilistic law, the distinction between them does not make much sense in the equilibrium distribution.

Four new t haplotypes, tTu1 through tTu4, are described, three of them derived from the tw12tf haplotype and one (tTu4) from the tw2 haplotype. The tTu1 and tTu4 haplotypes cause taillessness in T/tTu1 or T/tTu4 heterozygotes, lack the lethality factor, weakly suppress recombination in the T−H−2 interval, and are transmitted to offspring from tTu/ + males at nearly Mendelian ratios. The tTu3 haplotype resembles tTu1 and tTu4 except for the fact that the T/tTu3 heterozygotes have normal-length tails. The tTu2 haplotype probably carries the lethal factor of tTu12tf, suppresses crossing-over in the T-H-2 and tf-H-2 intervals, and displays a slightly subnormal transmission ratio. In the compound heterozygote tTu1/tTu2, the male transmission ratio of the tTu1 chromosome is close to that of the original tTu12tf haplotype. A similar effect is observed in the tTu3/tTu2 heterozygote. This observation is interpreted as evidence for two regions within the t complex controlling the male transmission ratios. One of the regions is close to the tail-modifying region, the other is close to the lethality factor. Our findings parallel closely those made in the segregation distorter system in Drosophila.

Recombinant-inbred (RI) strains of mice derived from the cross of strains C57BL/6J and DBA/2J were used to study the inheritance of susceptibility to cortisone-induced cleft palate. Most of the RI strains could be classified as either resistant, like C57BL/6J, or susceptible, like DBA/2J, suggesting the segregation of a major locus. An association with the phosphoglucomutase-1 locus (Pgm-1) on Chromosome 5 was observed. There was no association with the H-2 locus on Chromosome 17 as had been reported in previous studies utilizing different strains. We conclude that susceptibility to cortisone-induced cleft palate may be determined by different loci depending on the strains studied.

The duodenal mucosa of normal (+/+) and heterozygous tortoiseshell (Moto / +) female mice was analysed by an ultrastructural histochemical copper localization technique. Copper was rarely detected along the duodenal microvilli of + / + female mice. However, copper was localized on the surface of the brush border of the duodenal mucosa and within pinocytotic vesicles at the base of the microvilli of Moto /+ female mice. The mottled defect may involve a defective intestinal uptake of copper, as well as a faulty copper transport mechanism.

Mouse mutant genes which result in defects similar to those of medical importance in man may be of value as models for the study of the defect concerned. We report here a new gene causing congenital cataract in the mouse, which may be useful in the understanding of cataract in man.

A further point of interest is that Kratochvilova & Ehling (1979) have recently developed a new method of measuring increased mutation rates in the mouse, by examining offspring of animals treated with mutagens for the presence of cataracts due to mutant genes. For the purposes of this test it is valuable to have information on the number and map position of loci which can mutate to give cataracts.