An arg− conditionally Sm-dependent E. coli B strain became unable to grow on minimal agar containing low levels of Sm when the strain acquired an R factor which mediates Sm and Blu adenylation. The same R-containing strain, however, grew normally when Blu was substituted for Sm in the agar. The data strongly suggest that Sm-adenylate does not suppress the arg− phenotype in an in vivo system. The possibility that Blu-adenylate can cause phenotypic suppression without being bactericidal in vivo is discussed.

Nine methionine mutants of Aspergillus nidulans (six new mutants plus three isolated previously) were examined; five responded to homocysteine, none responded to cystathionine or cysteine.

Ten revertants of one of the mutants, methB3, blocked before homocysteine, were shown to be due to suppressor mutations. The suppressors were divided into six genes on the basis of complementation tests and recombination data. Mutants of two of the genes were semi-dominant in the heterokaryon but recessive in the diploid. Experiments in which conidial ratios in the heterokaryons were determined suggested that semi-dominance of these suppressors is due to a shift in nuclear ratios in the heterokaryon in favour of the suppressor nuclei.

Some of the suppressors were tested for suppression of two other methionine loci; they acted on methG1 blocked before homocysteine, but not on methH2 blocked after homocysteine, although four out of 13 crosses tested gave ambiguous results.

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.

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.

Cellular functions of a double mutant of Escherichia coli K 12 deficient in recombination (recA) and defective in excision of pyrimidine dimers (uvrB) have been compared to those of isogenic recA or uvrB single mutants and ‘wild type’ bacteria. A combined effect of the two mutations on cell survival both under normal conditions of growth and after exposure to ultraviolet light or mitomycin C was demonstrated. The ratio of optical density to the number of colony formers in growing cultures of the double mutant is three times greater than in similar cultures of the recA single mutant and 9 times greater than in either uvrB or in ‘wild type’ cultures. The doubling time in growing recA uvrB cultures is 90 min, compared to 60 min, for the recA single mutant and 40 min for the uvrB single mutant and ‘wild type’ bacteria. Growing cultures of recA uvrB (λcI857) bacteria contain a substantial fraction of cells which are unable to form colonies at 32 °C, but produce phage when heated to 42 °C. No such cells were found in cultures of the single mutants or the ‘wild type’ bacteria lysogenic for λc1857. The double mutant is 10 times more sensitive to ultraviolet light and twice more sensitive to mitomycin C than the recA single mutant. In contrast to recA bacteria, exposure of the double mutant to mitomycin C induces little additional breakdown of cellular DNA. Induction of the prophage by mitomycin C is, however, prevented in both recA uvrB (λ) and recA (λ) bacteria. Exposure to mitomycin C creates conditions which render the prophage inducible by a newly transduced ree A gene. This effect of mitomycin C persists and can be revealed in complete medium at 37 °C after 100 min of incubation. The decay of the prophage, in cells exposed to mitomycin C, proceeds at a similar rate in both the double mutant and the recA single mutant. The inability of recA lysogens to be induced to phage production is discussed in the light of the present findings.

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.

Certain drd mutants of fi+ R factors, when carried by strain HfrC, allowed polarized transfer of the Hfr chromosome to occur at the normal rate. These mutants were independently shown to be repressor-sensitive and so owed their de-repression to failure to produce represser (i−). With other drd mutants, independently shown to be repressor-insensitive (0c), the rate of polarized chromosome transfer was as low as with the wild type and only R pili were produced by the HfrC+ bacteria. These R factors, therefore, continued to produce repressor and the donor behaviour of an Hfr strain depends on functioning of the integrated F.

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.

F-like R factors are related to ColB-K77, but not to ColB-K98 or ColB-K166, by the criterion of superinfection immunity. Tests of de-repressed mutant R factors for susceptibility to repression by ColB-K98, known to produce represser for F, showed that these could be either repressor-sensitive or insensitive. The former were independently shown not to produce repressor, which was thus, presumably the reason for their de-repressed state.

An Arg− conditionally streptomycin (Sm)-dependent strain of E. coli B that carries an R factor mediating Sm adenylation cannot grow on minimal agar containing 20 μg Sm/ml unless the strain either becomes Arg+ or loses the ability to adenylate Sm (Harwood & Smith, 1969b). We have therefore studied the efficacy of this selection with respect to enriching for SmS mutants of such R factors. Following u.v. mutagenesis, cells were plated on the selective medium; of the clones which were examined, Arg− R-SmS colonies were found up to 3000 times more frequently than Arg+ R-SmR colonies.

By the use of pintail (Pt) and brown (b) as markers, the location of Mup-a, a locus controlling electrophoretic variation of one of the components of the major urinary protein (MUP) complex, on mouse linkage group VIII has been determined. The order and intervals determined from recombination frequencies in 121 offspring from a back-cross were Pt 4·1 b 6·6 Mup-a.

Chlosyne lacinia (Geyer) is a nymphalid butterfly ranging from the Southwestern United States and thence southward to Argentina (Ehrlich & Ehrlich, 1961). The insect is multibrooded and preferably feeds on sunflower (Helianthus annuus L.), although high populations have also been observed to be maintained on cocklebur (Xanthium saccharatum Wallr.).

A method has been devised for the selection of auxotrophic mutants in higher plants. The method depends upon the incorporation of BUdR into the DNA of non-auxotrophic cells and upon its lack of incorporation into the DNA of auxotrophic cells. A wide range of auxotrophic types were recovered.

In yeast it has been reported that some types of erythromycin-resistance are due to cytoplasmic genetic factors, localized in mitochondria (Thomas & Wilkie, 1968; Slonimski, 1969). In view of the current interest in genetical aspects of mitochondria, and the ease with which cytoplasmic heredity can be demonstrated in Paramecium aurelia, some tests have been made to determine whether erythromycin-resistant variants could be obtained in this ciliate and, if so, to determine their genetic basis.