The response to selection in any line depends on the size of the initial sample by which the line is founded. For a single locus with additive gene action the effects of number of founders on early rate of response and on final limits are studied in relation to selection intensity and number of parents in the selected line. The reduction in total response caused by a small number of founders is greatest for large populations under intense selection, especially when the desirable alleles are rare in the base population. If these alleles are at high frequencies it is possible that a line which has gone through a bottleneck may be more sensitive to a reduced population size during subsequent selection than a line which has not. Under some conditions replicate selection lines founded with small samples are likely to be less variable in response than lines founded with moderately large samples.

An investigation of the genetic aspects of fertility was conducted among inbred and hybrid generations of rats. The high-fertility LEW strain and the low fertility CAS strain were crossed and their hybrids inbred for four generations. Litter size, ovulation rate, sterility, and the weights of the thyroid, pituitary, adrenals, testes, seminal vesicles, ventral prostate, uterus, and ovaries were analysed in inbred and hybrid rats for evidence of strain differences and heterosis and in successive generations of sib matings for inbreeding depression.

CAS females produced smaller litters and had smaller thyroids, pituitaries, adrenals, ovaries, and uteri than LEW females. CAS males had larger testes but smaller adrenals than LEW males. Results of crosses included heterosis for female pituitary and ovary weights, but inbreeding depression for the weights of male adrenals, seminal vesicles, and ventral prostates, and female thyroids and uteri. Ovulation rate did not differ between strains and was not an important determinant of litter size in this study.

The decrease in litter size as a result of inbreeding was due partly to the inbreeding of the parents and partly to the inbreeding of the litter.

A subcellular dimension, the length of the spermatozoan midpiece, has been the subject of a two-way selection programme in mice. After thirteen generations of within-family selection the divergence between the selected lines amounted to 5·4 phenotypic standard deviations. The realized heritability was found to be 0·76 ± 0·02, dominance and commonenvironmental effects being apparently very small. The reality of the selection response was verified in measurements on live spermatozoa. Other measurements have shown that the change in the length of the midpiece has been independent of its width, and has occurred without a proportionate change in the length of the main-piece of the flagellum. An electron microscope study has shown that the selection has, in fact, brought about changes in the quantity of mitochondrial material in the sperm cells.

Comparison, by electrophoretic methods, of eel samples from Iceland, Scotland and Germany confirmed previous reports of uniformity in haemoglobin types. When liver esterases were examined, significant differences in the frequencies of phenotypes in the ‘fast’ zone of the electropherogram were found between samples from Germany and samples from Iceland and Scotland. The frequencies of transferrin phenotypes in Icelandic and Scottish eels differed significantly from those of French and American eels.

It follows that regional differences in gene frequencies probably exist within the species Anguilla anguilla. The implications for the ‘atlantic eel problem’ are briefly discussed.

Twenty-four mutants of Aspergillus nidulans were isolated which grew more slowly than normal on glucose as sole source of carbon and were unable to utilize intermediates of the tricarboxylic acid cycle. By complementation tests they were divided into five groups, each group representing a different cistron and the cistrons were assigned to linkage groups by mitotic analysis. The mutant loci have been designated sgp-1 to sgp-5 respectively. Three mutants have been mapped by meiotic analysis.

Data are presented which support the conclusion that in the flecked translocation, T (1; X) Ct, there is a spread of inactivation into both sides of the autosomal region inserted into the X. This would indicate that both parts of the divided X are subject to the X-inactivation process. The data also demonstrate that the inactivation of autosomal genes lying near each end of the insertion are modified by the X-chromosome controlling element system, Xce. Since the element modifies the heterozygous expression of X-linked genes on one side of the insertion, it would therefore be expected that it similarly modifies the heterozygous phenotypes of those on the other side. The data thus support the concept that the controlling element is the master gene, receptor site or inactivation centre which regulates the X inactivation process.

In mutants at the ‘bristle’ locus of Aspergillus nidulans the conidiophore remains as a stiff hypha rather than developing a vesicle, sterigmata and conidia. The brlA 12 allele of this locus has a variegated phenotype, and genetic analysis has shown that this is associated with a translocation which has a breakpoint in the map interval adjacent to the bristle locus.

The mutant phenotype is partially repaired on high-salt medium at low pH, and can also be repaired by suppressors, one of which has been mapped at a locus unlinked to brlA 12.

The mutant provides proof that variegation is due to instability of gene expression and not to mutability since brlA 12 is genetically stable and can be propagated from either conidia or sterile conidiophores, the structures formed at the two extremes of variegation, and the resulting colonies in both cases are identical to the original strain.

It has been shown by mitotic recombination that the translocation associated with the variegated mutant is a ‘simple translocation’ in which the distal half of linkage group VIII is attached to the end of linkage group III. This terminal attachment site does not appear to be damaged in any genetically detectable way.

Chromosome 5R of Secale cereale var. Imperial has been substituted for chromosomes 5A, 5B and 5D of hexaploid wheat. There is evidence of compensation, in terms of vigour, in all substitution lines. Chromosome 5R rectifies the male sterility of nullisomics 5A and 5D; however, it is unable to circumvent the meiotic irregularity and male sterility of 5B-deficient stocks. Another instance of wheat-rye chromosome pairing, in the absence of chromosome 5B, is reported. The data reported here demonstrate that the long arm of 5R is the more essential arm and indicate that chromosome 5R is homoeologously related to the group 5 chromosomes of wheat.

Plants of two rye genotypes, one highly inbred, the other not, were grown with varying amounts of available mineral phosphate. In two experiments, one using culture solutions, the other a field experiment, the results show an effect of phosphate treatments on mean chiasma frequency at first metaphase in meiocytes. Plants given increased amounts of phosphate showed an increase in chiasma frequency. A similar effect of phosphate on chromosome size and mass at mitotic metaphase in meristems is known and there may be a direct link between chromosome size and chiasma frequency.

Single ascospore cultures from triploids were screened as a potential source of disomic tester stocks for the purpose of genetical mapping of chromosomes in yeast. A high tolerance of aneuploidy was found, and strains disomic for only one chromosome were rare. There was a high occurrence of strains disomic at specific chromosomes and in certain multiple combinations of disomic chromosomes.

The colour difference (crimson and yellow) in Kerria lacca (Kerr) was used to test the ‘Lecanoid’ system of chromosome behaviour proposed on cytological evidence. The colour strains bred true for colour. Reciprocal matings between the colour strains produced only crimson sons and daughters, confirming that the colour difference is not sex-linked and that the male is somatically a diploid. The phenotypes of the F2 and the backcross generations differed according to the heterozygosity and the direction of cross of the F1 parents, since heterozygous females produced two kinds of gamete but heterozygous males produced only the maternal kind. Thus, while elimination of the paternal gene and hence chromosome was confirmed during the formation of male sex-cells, demonstration of somatic diploidy of the male is not compatible with a ‘Lecanoid’ system in K. lacca. Instead, the available cytogenetic evidence is suggestive of a chromosome system with heterochromatization and elimination of the paternal chromosome-set confined to the male germ line.

In the present study, skin fibroblasts and leukocyte cultures from patients with acute infectious mononucleosis were examined to determine if any in vitro marker chromosomes could be detected. No alterations in chromosomes could be found in fibroblasts either from the region of the typical rash or from other areas of skin. This would tend to suggest but does not necessarily prove that this tissue was not extensively involved in the disease process.

When a determinant for neomycin-kanamycin resistance (K) was transferred by an F-lac factor into Salmonella typhimurium, the resulting KF-lac strain was sensitive to the male-specific phage μ2 and F-lac was derepressed. However, F-lac alone is repressed in S. typhimurium. When kanamycin resistance is spontaneously lost from S. typhimurium KF-lac an element persists which derepresses F-lac in S. typhimurium. The results are consistent with the hypothesis that a locus der, for derepression of F-lac in S. typhimurium, lies on the K plasmid. The R factor Rldrd19 is derepressed in K12 but is repressed in S. typhimurium. It also is derepressed by der. In contrast to F-lac and R1, another R factor, R136drdH8, is derepressed in both K12 and S. typhimurium, so that the intervention of der is unnecessary for its derepression in the salmonella host.

Anomalous frequencies of transferrin phenotypes were found among the offspring of matings between deer mice heterozygous for the two forms of transferrin most common in natural populations. Matings involving other phenotypes produced offspring in the expected phenotypic frequencies. Selective penetration by facility, occurring only in the reproductive tract of the heterozygous females, appears to provide the most satisfactory explanation for the observations.

A mutation in Escherichia coli K12 giving resistance to about 5 μg/ml of streptomycin was found to be cotransducible by P1 with proA and proB, and is located at about 8·5 min on the chromosome map. The locus is named strB. A second mutation to the same resistance level was not cotransducible with either proA or proB and must be located elsewhere. Both mutations cause a marked increase in R-factor mediated streptomycin resistance, and significant decreases in resistance to several other antibiotics, both in the presence and absence of an R-factor determinant for the same antibiotic. The two mutations differ in their effects on bacterial sensitivity to crystal violet and EDTA.