Analysis of F1BC1 and BC2 progeny from matings of inbred DBA/2 and C57BL mice confirm the existence of a single major gene for C 57 BL-resistance to Friend virus. The doses of virus used did not obscure expression of this Mendelian unit.

Ca and P metabolism in the grey-lethal mutant mouse has been investigated. This animal is hypocalcaemic and hypophosphataemic and the serum alkaline phosphatase is elevated far above the normal. Increased bone ash content has been attributed to an elevated bone Ca. From in vitro experiments involving steady-state distributions of calcium and phosphate it is concluded that active bone metabolism is reduced in mutant bone. This reduced ratio may be attributed to an increased passive ion solubility.

These results tend to the assumption of an hormonal imbalance in this mutant system. An increased production of thyrocalcitonin has been postulated to account for these findings.

Genetic mapping of suppressors of the ilv-188 mutation is described. Suppressors of this mutation have been mapped at four ochre suppressor loci: sup L, sup M, sup N and sup O. The ochre suppressor described by Brenner & Beckwith is shown not to suppress ilv-188 whereas the suppressor described by the same authors suppresses ilv-188 and may represent the same locus as supO suppressors. The mapping by P1 transduction of the sup L, sup M and sup N loci is described.

A formal genetic analysis of the heterothallic, colonial green alga Eudorina elegans has been described. Wild-type strains were found to be sensitive to different drugs when grown on minimal agar containing very low concentrations of these drugs. Mutant strains resistant to high concentrations of drugs have been isolated. These are msr-500 (resistant to 500 μg/ml of DL-methionine-DL-sulfoximine), ery-r-100 (resistant to 100 μg/ml of erythromycin) and sr-100 (resistant to 100 μg/ml of streptomycin). The wild-type phenotypes sensitive to these drugs have been designated as mss-500, ery-s-100 and ss-100 respectively. The sr-100 also showed cross-resistance to other antibiotics belonging to the streptomycin group.

On genetic analysis, the msr-500 and ery-s-100 were found to be inherited in a Mendelian way. These alleles are not linked to each other or to the mating type locus. The inheritance of mating type was found to be due to a single gene difference.

The inheritance of ss-100/sr-100 was found to be non-chromosomal and was characteristically uniparental, always transmitted through the female parent. The evidence for the non-chromosomal gene (NC genes) controlling sr-100/ss-100 phenotypes in this organism has been derived from the exceptional zygotes in which the male parent apparently transmits streptomycin resistance to the progeny. Although ultraviolet or gamma-radiation resulted in normal survival curves of the exposed cells, no mutant deficient in any nutritional requirement was isolated.

Erythromycin-resistant mutants were separated into two categories showing Mendelian and non-Mendelian inheritance of resistance respectively. The cytoplasmic factor was located in the mitochondrion based on the fact that the loss of the mitochondrial genetic unit associated with the petite mutation (the ρ factor, assumed to be the mitochondrial DNA) resulted in a corresponding permanent loss of resistance. Conversely, the petite mutation in gene resistant mutants had no effect on the inheritance of resistance.

Analysis of vegetative and sexual progeny of isolated zygotes from a number of crosses between resistant and sensitive strains indicated that different mitochondrial types, both sensitive and resistant, co-exist in the yeast cell and are distributed at random among daughter cells under non-selective conditions. Only resistant mitochondria are in evidence if zygotes are put down to proliferate on medium containing the antibiotic.

Resistant strains were tested for retention of resistance following anaerobic culture (known to cause disruption of mitochondria). The cytoplasmic mutants retained their resistance but two gene-resistant mutants tested both lost their resistance. It was suggested in the latter case that resistance is dependent on the existence of intact mitochondrial membrane (possibly inner membrane). In the former mutants the mechanism of resistance may be the alteration of one or other of the components of the protein-synthesizing system of the organelle.

Twenty-four lines were bred from a base population of outbred Q mice by continued full-sib mating. Inbreeding did not cause depression in mean birth weight. However, convincing evidence of inbreeding depression in foetal weight at 17½ days' gestation was found; this depression in the rate of prenatal growth was attributable both to inbreeding in the litter and the mother. It was also inferred from the results of crossing the partially inbred lines that inbreeding in the litter caused depression of placental weight. It is concluded that the genes controlling the rate of prenatal growth exhibit directional dominance but that the resulting inbreeding depression in this trait does not lead to a lower birth weight, possibly because of the compensating effect of a longer period of gestation.

1. The maroon-like maternal effect, present when ma-l flies are bred from non-mutant mothers, is not found among the late emergents from normal cultures. The hypothesis that this is due to a deficiency of some nutrient(s) in old cultures is tested by growing larvae on defined, germ-free media with the nutrients reduced one at a time.

2. Omission of lecithin (but not reduction of casein, sucrose, RNA or cholesterol) decreases the percentage of maternally affected emergents, in proportion to the lowering of the lecithin supply. This is not a consequence of choline deficiency but of the shortage of fatty acids. Oleic, palmitic and linoleic acids can substitute for lecithin, when adequate choline is provided.

3. Pantothenic acid, nicotinic acid, thiamine and biotin deficiencies (but not reduced pyridoxine, riboflavine or folic acid) also lower the proportion of maternally affected flies. There is an interaction between pantothenic acid and lecithin, but not between lecithin and the other effective vitamin deficiencies.

4. Addition of the excretory product hypoxanthine to the complete diet significantly lowers the proportion of maternally affected emergents, but equivalent amounts of uric acid, or of guanylic acid, do not. It is argued that the quantitive relationships make it improbable that accumulation of excretory products play any great part in the disappearance of the maternal effect, whereas it is more likely that nutritional deficiencies do.

5. ma-l larvae grown on low lecithin have the same complement of xanthine dehydrogenase as those reared on normal lecithin. The lecithin effect is therefore assumed to operate by affecting the pattern of pteridine synthesis. Phenylalanine, which would also be expected to alter this pattern, modifies the maternal effect similarly.

1. Forty-nine auxotrophic mutants were isolated after irradiation with ultraviolet light. The biochemical requirements were identified and the response to possible precursors tested in some of them.

2. Diploid colonies were synthesized from compatible, auxotrophic haploid strains on an artificial medium by an adaptation of the balanced heterokaryon technique. Selection of diploid cells was especially convenient as the dikaryon cannot grow on such media, and is therefore only a transitory stage under these cultural conditions. Diploid cells were different in shape and size from haploids, and gave rise to colonies which could be distinguished by eye from haploids. The way in which diploid colonies arose from fusions between haploid cells was followed by microscopic observation. When known numbers of fused haploid cells were plated on minimal medium, diploid colonies occurred at a frequency of 3 × 10−4.

3. Diploid cells, heterozygous for mating-type alleles, were incompatible with either haploid mating-type (i.e. neutral).

4. Diploid cells could infect the host plant as a pure culture (i.e. they are solopathogenic).

5. Meiotic and mitotic segregation of the large-celled strains was used to confirm diploidy. Spontaneous mitotic segregation was very rare. Mitotic crossing-over was induced at a high frequency by irradiation of diploid cells with ultraviolet light. A convenient technique for induced haploidization was devised using p-fluoro-phenylalanine. Preliminary evidence using this technique indicates a haploid chromosome number of at least seven.

6. It is considered that U. violacea has many advantages as an organism for genetical research, especially for analysis of the parasexual cycle.

Cultures of Bacillus subtilis release transforming DNA during the early exponential and stationary phases of growth. The pattern of release of transforming DNA was followed by measuring transformation in a system consisting of a non-transformable DNA donor and a differently marked transformable recipient. Transformation in this system seems to be at least as efficient as that induced by purified DNA. Fluorescence microscopy revealed that released DNA remained bound extracellular to intact cells. The release of DNA during early exponential growth seemed to be correlated with the cells' proneness to lysis; both DNA release and cell lysis were inhibited by chloramphenicol. In stationary cells, the release of DNA was neither correlated with a similar proneness to lysis nor inhibited by chloramphenicol.

A chloramphenicol-resistant mutation in Escherichia coli K 12, cmlA1 (previously designated 1a), giving a higher Cm-resistance than other mutations yet examined, has been shown to have a chromosomal location, the gene order being gal, λ, bio, cmlA, pyrD. CmlA can be transduced efficiently into cm-sensitive strains by P1 with little phenotypic lag, and is co-transduced with the λ-attachment site (frequency 1·13%) but not with gal or pyrD.

Kojima's (1961) approximate formulae for the mean and variance of the change in gene frequency from a single cycle of selection applied to a finite population are used to develop an iterative method for studying the effects of repeated cycles of selection and random mating. This is done by assuming a particular, but flexible and probably realistic, approximate form for the distribution of gene frequencies at each generation.

The method gives for each generation the first two moments of the gene frequency distribution, the expected gain from selection, the probabilities of fixation and also the variability of gain. The variability of gain is of considerable importance in evolution, selection experiments and in plant and animal breeding programmes.

Kojima's (1961) formulae have been extended to allow for differentiation between males and females. Hence different selection intensities and population sizes for the two sexes can be studied. Selfing with selection is considered separately. Extensions to cover simple examples of multiple alleles, linkage and epistasis are possible. Reference is made to previous work using transition matrices.

Our previous research (Raicu & Bratosin, 1966; Raicu, Hamar, Bratosin & Borsan, 1967) has shown that the Romanian hamster (Mesocricetus newtoni, 2n 38) is a well-established species, differing considerably from the Syrian hamster and from other hamster species. The species is spreading in the south of Romama, especially in Dobrudja, and in Bulgaria. Its spreading area is completely isolated from the spreading area of all other species of Mesocricetus. The preferred biotops are uncultivated fields, dry steppes and fields cultivated with fodder plants. The Romanian hamster reveals important differences in the number and structure of the autosomes and in the degree of homology and presence of chiasmata in the heterosomes.

The three theories of dosage compensation in Drosophila are examined. Data are presented supporting a developmental interpretation. The reason why such a mechanism is applicable in insects but not in mammals is discussed.

A strain of S. typhimurium carrying transferable determinants, one for resistance to ampicillin (A), another for resistance to streptomycin and sulphonamides (SSu), was irradiated with ultraviolet light. A clone resulting from this treatment had lost streptomycin resistance and now carried the A determinant and a new determinant, ASu. Except for coding for ampicillin resistance, the ASu determinant was homologous with SSu. The A moiety of ASu produced ampicillin (penicillin) resistance of the same degree as the original A determinant. It was therefore concluded that irradiation had resulted in the elimination of the S gene in the SSu determinant and its replacement by an A gene to form ASu. Experiments with the ASu and SSu determinants suggest that there is normally only one copy of a resistance determinant in the host cell and only one cell site into which it can integrate.