Studies on the growth kinetics of R+ and R− cultures of Escherichia coli in the presence of nalidixic acid (NA), acriflavine (AF) and kanamycin (Kan) showed that each drug caused a decline in viability of both R+ and R− cells for several hours. During further incubation the viability rose rapidly for the R+ cultures, but either rose less rapidly (AF and Kan) or continued to decline (NA) for R− cultures. Distribution curves of the resistances of individual clones of R+ and R− bacteria to atabrine, NA, AF and Kan suggested that the presence of an R factor in the host bacterium increased its mutation rate to resistance to these drugs: this would account for the more rapid growth rate of R+ cells during the latter stages of incubation in their presence. The mutations causing increased resistance to NA and to Kan were located in the bacterial chromosome and not in the R factor.

By the use of appropriate strains of Escherichia coli, Shigella flexneri and Salmonella typhimurium with and without an R factor, R100, the mechanism of ‘curing’ of R factor by acridine dyes was examined. This R factor was shown to confer increased sensitivity to acriflavine upon the host cells. E. coli strain W-3630, once infected with R100, has never been observed to segregate R− cells. When mixtures of R+ and R− cells of this strain were grown in acriflavine broth, the proportion of R− cells increased and was also correlated with the proportion in the initial inoculum. Other bacterial strains carrying R100 segregate R~ cells spontaneously. Growth tests starting with varying proportion of R+ and R− cells of these strains in acriflavine broth also gave a marked correlation between the initial and final proportions of R− cells, and indicated that the main cause of ‘curing’ the R factor was the selective enrichment of R− segregants present in the initial inocula or arising spontaneously during growth of the R+ culture. These results suggest that the mechanisms underlying the ‘curing’ of F and R factors are different. Tests with several acridine dyes gave results similar to those with acriflavine.

Hybrids between four diploid species of Aegilops and species of Secale were obtained by using embryo culture. There was a marked incompatibility in the crosses between Secale species and each of the four species in Section Sitopsis of Aegilops and Ae. mutica. It is suggested that this genetic incompatibility with Secale species is an additional similarity between these species of Aegilops and the diploid species of Triticum.

Most chromosomes of Aegilops (A) and Secale (S) are univalent during meta-anaphase of meiosis in these hybrids, but some appeared to associate and others to pair as apparently normal chiasmate bivalents. Analysis of non-chiasmate and chiasmate associations showed that the frequencies of autosyndetic (AA and SS) and allosyndetic (AS) associations fitted the 3AA: 7AS: 3SS ratio expected if association and pairing is at random. Any deviations from random involved a deficiency rather than an excess of Aegilops-Secale pairing. There is no evidence that the chromosomes of Secale are homologous with those of Ae. caudata, Ae. comosa and Ae. umbel-lulata, and it is suggested that the genome of Secale species does not show any homology with the genomes of the genera Aegilops. This does not preclude the presence of homologous segments. It is suggested that the possibility of random association of chromosomes should be considered when occasional pairing in interspecific hybrids is analysed, and that identification of chromosomes and recognition of chiasmata are required. The possibilities of chiasmata between non-homologous chromosomes, of a genetic mechanism in rye which suppresses the pairing of homoeologous chromosomes, and of other factors causing asynapsis and pseudo-synapsis between genetically similar chromosomes are discussed.

Fifteen mutant strains of Chlamydomonas reinhardi were isolated which showed defects in some aspect of the process of cell-wall formation. Genetic analyses indicated that most of the mutations were due to single gene changes; two were anomalous in that non-Mendelian segregations were obtained on crossing with other genotypes, and on selfing they frequently gave rise to wild-type phenotypes.

Occasional somatic revertants were also obtained from these two strains. On the basis of these analyses it is suggested that there are two levels of control operating in the process of cell wall biogenesis - one concerned with subunit production at the nuclear level and another, possibly concerned with three-dimensional organization, at another level. Electron-microscope analyses of the different mutants showed the mutants to be divided into three main categories: those in which the wall was formed but was not attached to the plasma membrane, those in which the wall was attached to the membrane, and those in which very little wall was formed. In the last class in particular, vesicles containing wall precursors were clearly visible, and were shed through the plasma membrane into the medium.

Some quantitative implications of the gene conversion models of Holliday and Whitehouse & Hastings are discussed. These models predict two kinds of mispairing when a heterozygous mutant is in hybrid DNA. It is pointed out that the latter model, in contrast to statements in the literature, does not require identical repair rates in both kinds of mispairing.

Furthermore, some peculiarities are discussed which result if, among the corrected fractions of hybrid sites, the frequency of repair to wild-type is the same in both kinds of mispairing (r = s). In the Holliday model a minimum results under this condition for the frequency of asci which show a normal 4:4 segregation, but which have originated by repair from meioses with hybrid DNA.

A study of the structural and functional organization of the rudimentary (r: 1–54·5) locus of Drosophila melanogaster has demonstrated that alleles of this gene reside in a number of recombinationally separable sites, and display a complex pattern of interallelic interaction. Data relating to interallelic interaction have been utilized to construct a linear complementation map consisting of 7 complementation units and 16 complementation groups. Comparison of the genetic fine structure map and the complementation map shows that the two maps are approximately co-linear. Totally non-complementing alleles reside at both ends of the fine structure map. The r locus is best interpreted by the model of a single cistron whose product affects several distinct developmental processes and whose alleles display a complex pattern of interallelic complementation. Intragenic recombination within the r locus is accompanied by the appearance of parental and recombinant flanking marker classes not expected on the basis of reciprocal recombination. Studies with half-tetrads demonstrate that intragenic recombination can occur either by gene conversion or by a reciprocal exchange mechanism. The pattern of organization seen at the r locus is similar to patterns of organization found in work with fungal genes.

We found that la is located in linkage group XVIII. It is highly probable that la and tg are alleles, and closely, linked to Es-1. Mice of the genotype la/tg are abnormal, with clinical signs similar to tg, although more severe. They develop earliest signs at about 15 days of age, similar to la, are runted but fertile and can live for months. Clinical signs are ataixa, stiffness, retarded motor activity and intermittent focal seizures. The pathological basis for these symptoms is still elusive. The three types of mice, la/la, la/tg and tg/tg are thus distinct clinically, la/tg resembling in some respect either of the other two.

Derepressed mutants of F-like transfer factors, isolated by mutagenesis, were characterized as repressor-minus (i−) or operator-constitutive (oc). Mutants of the i− class are derepressed in K12 but repressed in Salmonella typhimurium. They are derepressed in S. typhimurium by a kanamycin resistance determinant carrying a locus der, described previously. Most oc mutants of F-like factors are derepressed in both K 12 and S. typhimurium. However, one mutant of F-lac was oc in K12 but was repressed in S. typhimurium. It was derepressed by der. Repression by S. typhimurium is different from that by fi+ factors, since der reverses the former but does not affect the latter. Possible interpretations of these findings are discussed.