The activity of several enzymes has been determined in the livers of homozygous obese and adipose mice, their normal litter-mates, and phenocopies induced in normal mice by aurothioglucose (ATG) injections.

Obese, adipose and ATG mice had higher activities of ATP citrate lyase, malic enzyme (NADP malate dehydrogenase) and pyruvate kinase than normal mice. Heterozygote activities are indistinguishable from wild-type. There was no difference between normal and fat litter-mates in the activity of malate dehydrogenase (NAD-linked), lactate dehydrogenase, isocitrate dehydrogenase and fumarase.

Crosses between mice doubly heterozygous for roth the ad and ob genes produced offspring that were only ‘fat’ or ‘normal’ and no offspring could be phenotypically recognized as the double mutant, either physically or in terms of ATP citrate lyase activity.

Gas–liquid chromatography of the fatty acids of the depot fat showed no differences between any of the types of litter-mate.

The alterations found in enzyme activity in obese and adipose mice are compared to several other enzyme activity differences reported in the literature for obese mice. These are discussed in relation to genetical criteria that may be estarlished to assess, from quantitative data, whether an enzyme is the site of the primary lesion in a mutant pheno-type. Some general observations are made on genetics and the control of metabolism.

Serum and urine samples from seven recombinant inbred mouse strains, derived from a cross between BALB/c and C57BL/6, were examined to determine the immunoglobulin heavy chain (IgCH) and the major urinary protein (MUP) allotypes. CXBG and CXBJ exhibited the same IgCH alleles as did BALB/c; the others resembled C57BL/6, thus providing no evidence of crossover types. Comparison of the Mup and brown coat colour (b) alleles (both on linkage group VIII) revealed that three of the strains resemble BALB/c and two resemble C57BL/6, whereas the CXBE and CXBI strains are crossover types.

The semi-dominant X-linked gene tabby (Ta) in the mouse and its recessive autosomal mimic crinkled (cr) produce the same mutant syndrome involving abnormalities of the hair, teeth and certain exocrine glands. Previous work has provided some indication of interaction between these loci in terms of vibrissa number. The results of the present study demonstrate that, for tooth size, mice doubly heterozygous for tabby and crinkled show a more extreme phenotype than either heterozygotes for tabby or crinkled alone.

Baker (1971) presented genetic evidence that the inviability of In(1)scL8/O and scS1/O males in Drosophila melanogaster is due to position effect suppression of ribosomal RNA cistrons. Although scL8/O and scS1/O males are inviable, scL8/scL8 and scS1/scS1 females are viable. We therefore asked the following question: Is scL8/O or scS1/O viable when part of a gynandromorph? In other words, is position effect suppression of rRNA genes autonomous or non-autonomous in gynandromorphs? In this paper preliminary evidence is presented which suggests that position effect suppression of rRNA cistrons is non-autonomous. The evidence is that scLS/ or scS1/O (male) parts of gynandromorphs are not only viable but normal in appearance.

The analysis of the variation in the mutation rate in the fractionated progeny of treated males, revealed a marked differential cell stage response to the various chemical series investigated. The mustard derivatives of amino-acids (particularly L-phenylalanine) exert their minimal mutagenicity on mature sperm, but possess an appreciable activity on other stages of spermatogenesis, including spermatogonia. The carboxylic-acid mustards produce their maximal effect on an early spermatid, but are practically ineffective on spermatocytes and spermatogonia. The amine mustard corresponding to the phenylalanine derivative is effective on the stages of spermiogenesis (including the early spermatids) as well as on the spermatocytes, but is inactive on the spermatogonia (at least the primary stages). The response of the gonia, therefore, is a function of the amino-acid moeity of the mutagen, and is not merely due to the presence of an amino-group in the molecule.

Thirty-two t haplotypes were extracted from wild mice captured in Central Europe, Spain, the Soviet Union, Israel, Egypt, the Orkneys and South and North America, and tested for lethality in the homozygous state. Twenty-two proved to be homozygous lethals, 8 semilethals and 2 viables. The lethal t haplotypes were then tested by the genetic complementation test for identity with representatives of known complementation groups and with each other. Five of the 22 haplotypes proved to carry previously identified lethality factors (tw5, tw73, and tLub-1), while the rest carried new factors. The 17 haplotypes fell into 8 new complementation groups. Two of the new groups are partially overlapping in that they seem to share some lethality factors and differ in others. These tests raise the total number of known complementation groups to 16. The distribution of the individual t haplotypes among wild mice populations seems to reflect their differentiation from a common ancestor haplotype.

Plasmids R68 and R68.45 were transferred from Pseudomonas aeruginosa to Escherichia coli by conjugation. R68.45 was able to mobilize the E. coli chromosome from different origins at a frequency of about lO−6/donor cell. With R68, no transfer of chromosomal genes could be detected. Plasmid R68.45 differs from its parent R68 only by an additional DNA segment, 2120 bp long, located close to the kanamycin resistance gene. By restriction enzyme analysis it was shown that the additional DNA segment of R68.45 is a duplication of a pre-existing DNA region of R68. The duplicated region is characterized by the following sequence of restriction sites: A–310 bp–SmaI–70 bp–PstI–795 bp–PstI–15 bp–KpnI–540 bp–HpaI–370 bp–B.

The endpoints A and B of the duplicated region were determined by a heteroduplex experiment between HindIII linearized molecules of R68 and R68.45. It is proposed that this duplication found in R68.45 is responsible for its chromosome mobilizing ability.

Hairs from two stocks of homozygous waved-2 mice have been examined. The observations do not agree with a previous report, that the waving was due to a decrease in the proportion of guard hairs and an increase in the number of constrictions per hair, but are consistent with the view that it arises from a defect of keratinization.

Segregation of sperm abnormality level and the pattern of major urinary proteins (MUPs) were investigated in F2 and B1 hybrid males obtained from crosses involving two contrasting inbred strains of mice: CBA/Kw (Mup-1a1a, 3·3% abnormal sperm) and C57BL/Kw (Mup-1b1b, 21·9% abnormal sperm). In the progeny of both crosses mean levels of abnormal spermatozoa were significantly higher for males typed as Mup-1b1b than for heterozygous Mup-1a1b males. Moreover, all F2 hybrid males showing very high percentages of abnormal sperm were Mup-1b1bhomozygotes. Similarly, among B1 males with a high level of deformed spermatozoa, a statistically significant majority were Mup-1b1b genotypes. Our results suggest that at least two genes which influence sperm abnormality level are segregating in these crosses. Both appear to be recessive for high sperm abnormality level, and one shows weak linkage to Mup-1 on chromosome 4.