Blood glucose levels of mice from five strains were measured. The results showed that each strain was different from the others for genes affecting blood glucose level, although the strain differences were small.

Within strains, the chief sources of variation were sex differences, differences between mice from different litters of the same mother, and between mice assayed in different months. Repeatability of measurements on individual mice was low. Genetic analysis, even by biometrical techniques, was not possible because the small genetic effects were obscured by variation due to other causes.

The advantage in using membrane filters for crosses between P+ (donor) and P− (recipient) strains of Vibrio cholerae (Bhaskaran, 1964; Bhaskaran, Sinha & Iyer, 1967) is probably due to more frequent and effective contacts between the cells on the surface of the membrane than is possible in fluid media with actively motile cells of this species. The transfer of the fertility (P) factor itself, as well as the yield of genetic recombinants, was considerably improved by this procedure.

Experiments were designed to investigate the effect of homozygous deletions upon the frequency and the average length of heterozygous regions in bacteriophage T4D. A long deletion, rdf41, which covers at least the whole rII region, was found to increase the heterozygosity for r48, while no increase was observed when a short deletion was employed. The long deletion was found to increase the average length of amber-HETs by a length approximately the size of the rII region.

A drastic reduction in average HET length was found in FUDR crosses homozygous for the long deletion rdf41, indicating that the type of HET that does increase in FUDR is very short.

In the cross with no deletion in either parent, premature lysis HETs were found to be much longer than normal lysis HETs. Assuming that redundancy HETs are long compared to heteroduplex HETs this result indicates that redundancy HETs are made earlier in the latent period than heteroduplex HETs. A fluctuation in HET frequencies was found for different markers, especially in FUDR.

About half of all HETs, both in normal crosses and in FUDR crosses, was found to be parental for outside markers.

In non-FUDR crosses, polarized segregation was shown by 12 out of 27 multi-marker HETs after normal lysis and 5 out of 22 multi-marker HETs after premature lysis. In FUDR crosses, 24 out of 77 multi-marker HETs showed polarity.

Four white-spored allelic mutants of Ascobolus immersus were used to study the effect of mutant and cross specificity on the recombination pattern in intragenic crosses.

In the locus studied no correlation was found between the position of mutants on the map and their basic conversion frequencies. One of the mutants evidently caused an increase of conversion frequency of the two others. Crossing-over in intragenic recombination may be mutant-specific as revealed by using two mutants which give no recombinants when crossed with each other. The frequency of crossing-over was higher in crosses in repulsion than in coupling involving the same pairs of mutants. Polarization observed in two-point crosses was due in some instances predominantly to differences in basic conversion frequencies of the mutants used, and in others to the relative position of the mutated sites. Mutants located in the central part of the studied region were those which converted most frequently in two-point crosses. No reciprocal conversions were observed.

A number of recombinant asci resulting from two or more separate but highly correlated recombinational events within a gene were found.

The frequency of cotransduction of motC and H1 in Salmonella has been investigated, using four Salmonella serotypes and many serotypic recombinants as donors and S. typhimurium motC mutant as recipient. The frequency varied with the four serotypes from 7% to 52%. It is suggested that the difference in frequency arises from not only differences in genetic homology between the chromosome of the recipient and the fragment from the donor, but also from differences in genetic composition of the chromosome fragments carried by the phage. The frequency of serotypic recombinants selected for motC+ and H1 gene of the donor is generally higher than with recombinants selected for flaK+ and H1. The difference in genetic homology between S. typhimurium and other species is more marked in the region between H1 aud flaK than between motC and H1.

The gene pn was found to be active already in larvae 30 h old, long before eye-pteridines accumulated. At this developmental stage pn interacts with the gene K-pn. From studies with induced somatic recombination, gynandromorphs, and induced pn mutations, in a K-pn background it was concluded that the interaction pn-K-pn is non-autonomous in the epidermis, but in some internal organs it is apparently autonomous and causes the death of pn–K-pn flies. It is proposed that pn mutants interfere with an early step of the conversion of guanosine to pteridine, so that a deficiency of drosopterines, but not of the competing sepiapterine and biopterine, is caused. The accumulated precursor is presumably the substrate for a poisonous reaction triggered by K-pn.

Previous studies had shown that haploid strains of Aspergillus nidulans which have a chromosome segment in duplicate are unstable at mitosis. Through the study of various haploid and diploid strains, with and without translocations and with balanced and unbalanced genomes, it has been shown: (1) that imbalance of chromosome segments is responsible for instability, and (2) that the chromosomal deletions produced are confined solely or largely to the segments which provoke instability.

The term ‘mitotic non-conformity’ has been proposed for this instability phenomenon. An explanation for it has been sought in terms of attachment sites, limited in number and specific for chromosome segments, at which replication is initiated.

When killer and neutral strains of Saccharomyces cerevisiae are crossed the resulting diploid clones possess a killer phenotype and when spored yield a complete range of tetrad ratios.

The combined results of analysing tetrads and vegetative cells of diploid clones derived from two different neutral × killer crosses (K1 × N1 and K2 × N1) demonstrate that the range of tetrad ratios can be accounted for by the occurrence of somatic segregation of killer (k) cytoplasmic determinants prior to sporulation. Such results support the genetic model for the inheritance of the killer character in yeast already proposed (Somers & Bevan, 1969).

During the course of these studies a correlation was found between the strengths of the killer phenotypes of diploid colonies and the proportions of killer spore cultures obtained after sporulation of their cells.

Conjugation brought about by each of eight different R factors was as efficient as with F in the production of genetic recombinants for a variety of genes located throughout the chromosome of Escherichia coli K12.

A method for concentrating flagella-paralysed (mot−) cells existing in a large number of non-flagellated cells of Salmonella was invented. The mot− cells expressing the phase-1 flagellar antigen i were agglutinated by anti-i serum with carriers, the dead cells of TM2 expressing the phase-1 antigen i; only the agglutinated cells were harvested by a low speed of centrifugation and incubated in broth. About tenfold concentration was brought about by one treatment, which was repeated for further concentration. By this method, the motA257 motC244 double mutant which was produced by transduction at a frequency of about 3 × 10−6 per non-flagellated recipient cell was isolated from the broth culture concentrated five times, in which about 30% of the cells were the double mutant.

Two allelic forms of the supernatant NADP isocitrate dehydrogenase (IDH) are found in inbred strains of mice (Henderson, 1965). The five C3H substrains tested, namely C3H/HeJ, C3H/Re-sl, C3H/N-wJ+, C3H/J-WX+ and C3HeB/FeJ, all proved to be of the Id-la/Id-la genetic constitution. (For the nomenclature of inbred strains and substrains of mice see Staats, Committee on Standardized Nomenclature for Inbred Strains of Mice, Cancer Res. 24 (1964), 147–168.) All these substrains were obtained from E. S. Russell at the Jackson Memorial Laboratory, Bar Harbor, Maine, and were presumably all derived from C3H/He mice.