A simple method is given to compare the relative fitnesses of various populations of one species when they compete with another species. Populations of Drosophila psevdoobscura polymorphic for the chromosomal inversions CH and AR are superior to monomorphic populations CH or AR when they compete for the available resources with D. serrata.

N-methyl-N′-nitro-N-nitrosoguanidine treatment of a donor strain of Pseudomonas aeruginosa resulted in the isolation of strains which were presumably cured of their sex factors, strains which possibly contained mutant defective sex factors and one strain which showed enhanced donor activity. The latter was apparently due to a change in the bacterium and the sex factors of OT 302 and OT 15 were both shown to be similar to the original in OT 1 when the three were transferred into the same strain.

The effect of nalidixic acid, a specific inhibitor of DNA synthesis, on Escherichia coli strain B (lon) and its u.v.-sensitive derivatives is examined. Strain B itself is sensitive to nalidixic acid, whereas its u.v.-resistant derivative B/r is resistant.

It is shown that in all exr A strains, in which u.v.-induced filamentation is suppressed, resistance to nalidixic acid is increased. Among exr A strains, Bs4 is exceptionally resistant to nalidixic acid. This is because nalidixic acid kills only growing cells and strain Bs4, a try auxotroph, may grow poorly under the conditions used to test nalidixic acid.

The uvr genes of the HCR strains Bs1, Bs8 and Bs12 do not suppress u.v.-induced filamentation nor do they affect the response to nalidixic acid. The uvr gene of strain Bs3 is unusual in increasing the tendency to filament and also sensitivity to nalidixic acid.

Strains Bs1, Bs3 and Bs8 are all doubly mutated from strain B, the second mutation (not uvr) being responsible for their increased resistance to nalidixic acid as well as partially or completely suppressing filamentation.

It is concluded that the cell division mechanism of (lon) strain B is sensitive to inhibition of DNA synthesis. Mutations which suppress the tendency of strain B to filament reduce its sensitivity to inhibition of DNA synthesis.

Evidence is presented which indicates that the phenylalanine analog 2-amino-3-phenylbutanoic acid (APBA) induces mutation to APBA, streptomycin, and neamine resistance in the green alga Chlamydomonas eugametos. Apparent chromosome abnormalities (reciprocal translocations and inversions) were also found among some clones recovered after APBA treatment. The two, mutation and chromosome aberration, are separable.

Strains of Aspergillus nidulans with a chromosome segment additional to the normal complement are vegetatively unstable. Previous work suggested that the deletions occurring at mitosis were confined to the unbalanced segments. It has been shown now that deletions, while probably always involving a duplicate segment, may extend beyond it to produce hypohaploids and hypodiploids, respectively, from unbalanced haploid and unbalanced diploid parents.

Hypoploids have been proposed tentatively as an explanation for some cases of phenotypic variegation; on this basis it is possible to account for some of the diverse phenomena shown by, for example, position-effect variegation.

Morphology and the rate of RNA synthesis of the X-chromosome in XX/XO mosaic larval salivary glands of Drosophila melanogaster have been examined. For this purpose the unstable ring-X was utilized to produce XX and XO nuclei in the same pair of glands. The width of the X-chromosome and the left arm of the 3rd chromosome (3L) of larval salivary glands was measured and the rate of RNA synthesis by them was studied upon the use of [3H]uridine autoradiography in such XX (female) and XO (male) nuclei developing in a female background (i.e. otherwise genotypically XX). In such mosaic glands the width of the single X-chromosome of male nuclei is nearly as great as that of the paired two X's of female nuclei, as is also the case in normal male (X Y) and female (XX). The single X of male nuclei synthesizes RNA at a rate equal to that of the paired two X's of female nuclei and nearly twice that of an unpaired X of XX nuclei. Neither the developmental physiology of the sex nor the proportion of XO nuclei in a pair of mosaic salivary glands of an XX larva has any influence on these two characteristics of the male X-chromosome.

It is suggested that dosage compensation in Drosophila is achieved chiefly, if not fully, by a hyperactivity of the male X, in contrast to the single X inactivation in female mammals, that this hyperactivity of the male X is expressed visibly in the morphology and metabolic activity of the X-chromosome in the larval salivary glands of the male, and that this hyperactivity and therefore dosage compensation in Drosophila in general is not dependent on sex-differentiation, but is a function of the doses of the X-chromosome itself.

Temperate phages φ 80 and λ grown in E. coli strain C differ markedly in the degree to which they are restricted by E. coli strain K. The basis of this difference is subject to genetic recombination and deletion. The loss of restriction sensitivity by deletion shows that sensitivity is determined by loci in the phage genome. These loci are interpreted to be targets of the restriction mechanism, in agreement with previous biochemical evidence.

In Escherichia coli the u.v. sensitivity gene recA suppressed u.v.-induced filamentation in a lon u.v. sensitive strain without affecting capsular polysaccharide production. recA appears to prevent the stimulus that leads to filamentation in a lon strain.

The autosomal recessive gene muted, mu, which arose spontaneously, dilutes coat and eye colour and causes absence of otoliths in some but not all homozygotes. Its locus is in linkage group XIV of the mouse, and the order of loci was shown to be bg–Xt–sa–mu–f–pe.