1. By the use of intervarietal chromosome substitution lines, the poor crossability with rye (S. cereale, 2n = 14) of the wheat (T. aestivum, 2n = 42) variety Hope was shown to be determined by chromosomes 5A and 5B. The genes Kr1 and Kr2, which are responsbile for poor crossability (Lein, 1943), are probably located on chromosomes 5B and 5A respectively.

2. Crossability is actively inhibited by the dominant alleles, Kr1 and Kr2, of Hope and is apparently not enhanced by the recessive alleles, kr1 and kr2, of the readily crossable variety Chinese Spring.

3. The inhibition of crossability with rye conferred evolutionary and agricultural advantage upon wheat by preventing the production of sterile wheat-rye hybrids which could be regarded as weeds generated from within the crop.

1. The linkage order of four tryA mutants of S. typhimurium, and cysB-12, is:

Attempts to plot the position of tryA-50 were unsuccessful.

2. Some of the reversions of tryA-8, tryA-47, tryA-56 and tryA-50 were analysed genetically; tryA-52 does not revert. All four auxotrophs gave reversions that were phenotypically and genetically indistinguishable from that expected by back-mutation of the original mutant site.

3. Both tryA-8 and tryA-50 produced reversions that grew as wild-type but were due to unlinked suppressor mutations. Some of these were super-suppressors in that they suppressed both tryA-8 and tryB-4; others suppressed many site mutants in the tryA gene but did not suppress tryB-4.

4. All the slow-growing reversions of tryA-8, tryA-50 and tryA-56, and a minority of the semi-fast reversions of tryA-8, were due to unlinked suppressors.

5. All the slow-growing reversions of tryA-47, the semi-fast reversions of tryA-56 and the majority of the semi-fast reversions of tryA-8 were due to genetic changes that were inseparable, in very extensive experiments, from their original mutant site.

6. Slow-growing reversions of tryA-47 produced faster growing mutants. Some of these were due to mutation in unlinked modifying genes and in others the genetic change was within the tryA gene. Nine of the latter had the genetic change just to the left of the 47S site; in one the change was inseparable from the 47S site. None had this further change to the right of the 47S site. These further changes, in the absence of the 47S site, gave prototrophic phenotypes; they are inter-site suppressors.

An LT2 Hfr strain, his metC gal, was crossed to a multiply marked LT2 F− line. Analysis of recombinant yields, segregation of unselected markers and interrupted matings indicated injection of the Hfr chromosome in the sequence

The introduction into the Hfr of the colicine factors colI, colE1 and colE2 and the R factor R2 had little or no effect on its fertility. All four factors were transmitted at low frequency to the F− population, and to recombinants at higher frequencies (colI 5–30%, colE1 30–80%, colE2 5–30%, R2 0–9%). Transfer of colE1 occurred before 20 min., that of colE2 and colI later than 100 min. Segregation data did not reveal close linkage of any factor to any chromosomal locus, but recombinants with a long stretch of donor chromosome were more likely than others to have acquired colE2 and colI. Nearly all recombinants and F− cells which acquired colI or colE2 acquired both, and colE1 also. Most cells which acquired R2 acquired one or more colicine factors. These plasmid associations can be formally represented by transfer of plasmids, independently of the chromosome, in the sequence colE1—(colI, colE2)—R2. Phage P22 grown on the Hfr carrying the four plasmids transduced the tet-r trait of R2 at very low frequency, and the sul-r str-r characters, together, at low frequency. Some of each sort of drug-resistance transductant, but no transductants in respect of chromosomal characters, acquired colEl or colE2 by co-transduction.

Nineteen axial skeletal variants are described in the frog Rana cyanophlictis, collected from five isolated populations of Delhi. Four of these populations came from large perennial ponds and one, a transitory population, was entrapped from a temporary rain pool. The populations were found to diverge significantly from each other in the incidence of these skeletal variants. We have attributed this divergence to genetic drift, but the effects of unknown selective forces cannot be ruled out.

Parameters necessary for predicting direct and correlated responses for large and small 13-day larval weight in T. castaneum on two levels of nutrition were estimated in the base population. Larval weight in the GOOD environment was approximately twice that observed in POOR. Heritabilities (estimated from the ratio of sire component to total phenotype variance) of larval weight on the two rations were similar, 0·21 ± 0·06 and 0·19 ± 0·05 for GOOD and POOR, respectively. Heritabilities based on dam-offspring covariances were similar to these, but those obtained from full-sib covariances were much larger (0·97 ± 0·07 for GOOD and 0·69 ± 0·07 for POOR). This suggested that considerable dominance rather than maternal effects were present. The genetic correlation between growth on GOOD and growth on POOR was estimated as + 0·60 ± 0·21.

The selection experiment was replicated four times with each replication extending over eight generations. Good agreement between predicted and observed values for direct selection was observed for large selection in both environments and small selection in POOR. However, response to small selection in GOOD was significantly greater than predicted in all four replications and was associated with increased selection differentials. Realized heritabilities were approximately the same for both directions in GOOD yet asymmetrical responses occurred for all replications due to unequal selection differentials. On the other hand, realized heritabilities were asymmetrical in POOR. Those observed for small selection were more than twice the size of those calculated for large lines. However, the responses in POOR were symmetrical since the selection differentials varied inversely with the realized heritabilities.

Because of the asymmetry observed for heritabilities and selection differentials, correlated responses were poorly predicted. The average effective genetic correlation between growth in GOOD and growth in the POOR environment agreed remarkably well with the base estimate, yet asymmetry of the genetic correlation was a consistent phenomenon with values for the large lines being less than the base parameter while small lines were uniformly larger.

Asymmetries of the various genetic parameters were not anticipated from base estimates. They were not caused by sampling or chance fluctuations since all four replications were remarkably consistent. Asymmetry for any one genetic parameter (e.g. heritability) was associated with a particular environment or direction of selection while other genetic parameters reacted asymmetrically in populations exposed to a different set of environmental treatments.

For maximum performance in a single environment, these results show that selection should be practiced in that environment. With regard to mean performance in GOOD and POOR environments, selection for large size in POOR gave some 25% more gain than selection in GOOD. Selection for small size in either environment was equally effective in obtaining minimum size in both environments.

1. By means of tetrad analysis three vitamin-requiring mutants have been established as markers of centromeres distinct from those of the two known chromosomes.

2. Mutants existing in stock were tested for linkage with these centromere markers, and four previously unknown linkage groups with independent centromeres thereby established and accurately mapped.

3. Corrections were made to the maps of existing linkage groups. The A locus (Group I) was shown to be approximately four times as distant from its centromere as hitherto supposed (at least in most crosses); and several markers of Group II were mapped for the first time.

Contrary to opinions expressed by various authors, the phenotype of heterozygotes for mammalian sex-linked genes gives no support for the Lyon hypothesis (L.H.). Evidence, mainly from the mouse, shows that in such heterozygotes, both alleles act together as in autosomal genes.

In the present paper, it is shown that neither the behaviour of double heterozygotes for sex-linked genes nor that of X-autosome translocations provides independent evidence in favour of the L.H.: in each case, the interpretation depends on that of the behaviour of single heterozygotes and hence fails to discriminate. Moreover, new facts from both types of situation are also contrary to the L.H. In particular, a unified interpretation which fits the behaviour of genes in all known types of X-autosome translocations in the mouse requires the assumption that partial inhibition of gene action happens in both X-chromosomes of mouse females, and presumably the females of other mammals. The new hypothesis is consistent with all relevant genetical facts and, like the L.H., it also accounts for dosage compensation.

The kinetics of spread of colicin factor Ib (colIb) in col− cultures of S. typhimurium was studied. The rate of spread was greater with pil+ strains (those forming common pili) than with pil− strains. The difference reflects inefficient pairing between pil− cells, which donate or receive colIb efficiently only when mated with pil+ cells. The donor function of colIb is known to be repressed a few generations after it is acquired by a col− cell. While donor ability is manifest, a new type of pilus (the ‘Ib pilus’) is formed which is morphologically distinct from common pili and other sex pili such as that determined by the F factor. The Ib pilus is presumably involved in the transfer of colIb by conjugation.

Additional data are presented on the maintenance of kappa particles in cells of P. aurelia (stock 51) after removal of the gene K. It is shown that kappa particles may be maintained for as long as twenty-seven fissions in the absence of K, or may disappear before eight fissions. Slight retardation in fission rate of paramecia quickly eliminates kappa particles. The bearing of these results on the metagon theory is discussed.

A lysogenic, recombination-deficient bacterial mutant (rec−) can be induced to produce λ ind− C587 by a temperature shift, although it does not produce phage after u.v. irradiation when lysogenic for wild λ. When this mutant (rec−) was made colicinogenic for colicins E2 and I, colicin production was found not to be inducible.

Superinfection of irradiated lysogenic rec− (λ) bacteria, at doses of irradiation that did not reduce their capacity to produce phage λ, was not productive. It seems therefore that a certain product(s) that usually arises following u.v. irradiation in rec+ cells, and triggers the induction of lysogenic and colicinogenic cells by causing loss of immunity or repression, is not produced in the rec− mutant. However, immunity is lost and the prophage is induced after a temperature shift in rec− cells which are lysogenic for λ ind− C857.