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.

In mice heterozygous for translocation T(2;?)163H, and also for linkage group II markers, the cw locus shows close linkage with the point of rearrangement (about 1−2% recombination). Since T 163 was apparently formed by fusion of two chromosomes near their centromeres, this means that the centromere must lie at the cw end of linkage group II. In homozygotes for T(2; 9)138Ca the genes T and d show significant linkage, indicating that their loci are on opposite sides of the trans-location break. Since, from previous data, the break is known to be proximal to d, it must then be distal to T and, again from previous data, the order of loci hi linkage group IX must be centromere-T-tf-T 138 break.

Electrophoretic studies on starch gel demonstrated the existence in the European eel of four haemoglobins, not two as believed from agar gel studies. The two minor fractions have been shown to be neither polymers nor methaemoglobin derivatives of the two principal fractions.

The esterase zymograms of eel sera exhibit up to eight fractions. The individual differences observed suggest genetic polymorphism and the same applies to the esterase pattern of various tissues.

This approach is of value for the collection of phenotypic frequency data with a view to solving the Atlantic eel problem.

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.

Two triplications induced in a normal halpoid chromosome complement by TEM (Tr-I) and by mustard gas (Tr-II) are described. Two models which may lead by successive steps to the formation of a triplication are suggested. The induction of two latent breaks is essential in both of them. The origin of repeats in general is discussed. It is concluded that chromosome breaks rather than non-homologous crossing-over constitute the major source of repeats.

A simple technique for the selection of auxotrophs of Penicilhium chrysogenum after mutagenic treatment has been devised using nystatin. It relies on the differential sensitivity of germinated and dormant conidia to nystatin and on the gradual loss of antibiotic activity which occurs on complex media at laboratory incubation temperatures. After mutagenic treatment, conidia were plated on MM agar to allow germination of prototrophs and then overlaid with CM agar containing enough nystatin to kill germinated conidia but not ungerminated auxotrophic conidia. When nystatin activity had decreased sufficiently the latter germinated and grew and thus were enriched relative to prototrophs.

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.

Two new wild strains of T. pyriformis, syngen 1, have been examined for new matingtype, serotype and isoenzyme alleles. No new alleles at the mating type (mt) locus were found, but the two alleles previously found were extracted. No new alleles were found at the other five loci examined, but two alleles were obtained for each locus. These observations indicate that a limited polymorphism exists for these loci in natural populations of T. pyriformis, syngen 1.

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 extent of certain rII deletions in phage T4 has been mapped by genetic means beyond the terminus of the B cistron. They extend to varying degrees, nearly to the acs locus. The phenotypes of these mutants indicate that there are two or three cistrons between rII B and acs, and that the functions coded for by these cistrons are not essential for growth in any known E. coli K12 strain or E. coli lysogen.

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.