Maximum likelihood estimates of codon and base frequencies from observed amino acid composition of proteins were obtained based on models capable of revealing dependency between base arrangements in the three positions of a codon. Results showed that many of the proteins analysed revealed dependency between base arrangements in the first and second codon positions (first-order interaction). Also, in a number of proteins the interactions between base arrangements seemed to involve simultaneously more than one first order interaction and/or a second-order interaction (among base arrangements in the three codon positions). It was of interest to observe that the model of random base arrangements did not fit the observed amino acid data in almost all of the proteins that were analysed. More than ten amino acids contributed to this deviation from randomness.

Complementing diauxotrophic mutants of P. glycinea were mated in combination in which one or both mutants contained a resistance plasmid. The transfer of chromosmal markers was scored by the appearance of prototrophy at one or more of the auxotrophic loci. The resistance plasmid RP1 was equally or slightly more efficient than R6886 in the transmission of chromosomal genes.

Two reciprocal mouse translocations T(2; 8)26H and T(1; 13)70H, heterozygous in a Swiss random-bred background, show differences in the spectrum of multivalent configurations and in the segregational behaviour of these multivalent configurations. T26H/+ males mostly contained rings of four (R IV, 53·15%) and T70H/+ males chains of four, missing a chiasma in the shortest interstitial segment (C IV 11, 61·55%). The adjacent II frequency, estimated from metaphase II observations, was 8·47% in T26H/+ and 25·22% in T70H/+. Univalents of the shorter translocation chromosome of T70H are able to divide equationally at first anaphase. The hypothesis is advanced that time differences in chiasma terminalization during metaphase I-anaphase are important for explaining the difference in segregation observed between the two translocations. Translocation-caused non-disjunction is probably low in T26H/+ and 4–5% in T70H/+. Univalents involving T70H/+ are usually capable of co-orientation with the other chromosomes of the translocation complex. The summed percentages of adjacent II disjunction and non-disjunction caused by the translocations were estimated from the relative fertility scores of T/+ males and females versus +/+ males and females as 9·8% and 29·0% for T26H/+ and T70H/+ males, respectively, and 9·4% and 27·8% for T26H/+ females and T70H/+ females. For both translocations, the agreement between the various estimates is good. Chiasma frequencies are much higher in telomeric segments than in proximal segments containing centric heterochromatin.

Two pairs of lines of mice, selected for High and Low weight at 5 weeks of age (H5 and L5) and at 10 weeks of age (H10 and L10) over 15 generations, were compared with each other and an unselected control line (QC) at three different ages, i.e. at 5, 10 and 21 weeks of age. Differences in percentage fat between High and Low lines were small at 5 weeks, clearcut at 10 weeks and at 21 weeks the High lines were almost twice as fat as the Low ones. The H5 line was slightly fatter than the H10 line at all three ages and the L10 line was fatter than the L5 line at two ages. The developmental pattern of fat deposition was unaffected by selection for high or low weight at 5 weeks, i.e. the relationship between fat weight and carcass weight was similar in the H5, L5 and QC lines. Selection at 10 weeks affected the level of fat at low carcass weights and the relative rate at which fat was subsequently deposited. The different correlated responses resulting from selection at 5 and 10 weeks are explained in terms of genetic variation in (1) the rate of food consumption, (2) the efficiency of energy utilization for growth, and (3) the relative amount of fat deposited up to the age at selection.

The TOL(M1) metabolic plasmid was transferred from Pseudomonas arvilla mt-2 to a mutant of Pseudomonas putida. Although neither the donor nor the recipient could grow on phenol, the transconjugants could grow slowly on this carbon source. In these transconjugants phenol was converted to catechol by chromosomal encoded phenol hydroxylase followed by degradation of catechol by low uninduced levels of the plasmid encoded catechol meta cleavage pathway. A mutant, which grew well on phenol, was isolated from one of the transconjugants and it was found that phenol could now act as an inducer for the meta cleavage pathway.

Detailed physiological and genetic studies of haploid and diploid strains have revealed a complex phenotype for the rec-1 mutation in Ustilago maydis. The mutant is defective in the repair of damage by UV light, ionizing radiation and nitrosoguanidine. Four alleles are all recessive and have the same sensitivity to UV, suggesting the loss of a single cellular function. A significant fraction of non-viable cells is formed during growth, and in diploid strains considerable variation in colony size and morphology is seen. The spontaneous frequency of mutation is greater than in wild-type cells, but there is little, if any, enhancement by irradiation.

rec-1 also has pleiotropic effects on genetic recombination. The spontaneous level of mitotic allelic or non-allelic recombination is abnormally high, but the relative increase after irradiation is much lower than in control diploids. Allelic recombination is strongly associated with the expression of a hetozygous recessive distal marker, and it is shown that this is often due to hemizygosity rather than to homozygosity of this marker. The results indicate that allelic recombination is due to crossing over rather than gene conversion, but that the cross over is often associated with a chromatid break. rec-1 interacts with other radiation sensitive mutants, such as rec-2. Diploids homozygous for both are totally deficient in allelic recombination. In crosses between rec-1 strains meiosis is defective, with a low viability of meiotic products and frequent production of aneuploids or diploids among the survivors. The overall phenotype of rec-1 strains can best be explained in terms of the loss of a regulatory function, which leads to uncontrolled recombination during mitosis and meiosis, and the loss of a recombination repair pathway which is normally induced by agents which damage DNA.