A selection experiment for sternopleural bristles in Drosophila melanogaster was undertaken to measure the effect of suppressing crossing-over on chromosomes II and III using the inversions Curly and Moiré marked with a dominant gene, which severely reduce crossing-over. In one set of lines selected wild-type males were mated to selected females, heterozygous for Cy and Mé, and in a parallel set selected males carrying the inversions were mated to selected wild-type females. Because there is no crossing-over in the males in this species, crossing-over is much reduced in the first set and is at its usual level in the second. The effect of the selection was measured on flies which did not carry the inversions. The suppression of crossing-over reduced the advance at the limit by 28 ± 8% for selection upwards and by 22 ± 7% for selection downwards. The segregation ratios of the inversions were observed throughout the experiment. At the end, the proportion of wild-type flies emerging was not different in the two sets of lines. The results are consistent with an assumption of initial linkage equilibrium between loci affecting sternopleural bristles in the base population.

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.

Genetic mapping by means of mitotic haploidization (induced by parafluoropkenylalanine) and mitotic crossing-over was carried out with the fission yeast Schizosaccharomyces pombe. Thirty-two different genetic markers were involved in this investigation; some meiotic linkage relationships had been previously reported (Leupold, Megnet) for 16 of these loci. Mitotic haploidization experiments resulted in the genetic identification of six chromosomes in the haploid complement.

Furthermore, in an attempt to study the mechanism of action of parafluorophenylalanine (pFPA) on mitotic haploidization, pedigree analyses were performed by micromanipulation of diploid cells growing in the presence of pFPA. Haploid cells were detected after 40 hours of contact with the analogue and many lethal pedigree branches were observed. These observations seem to agree with Käfer's (1961) and Lhoa's (1968) suggestion that mitotic haploidization in Fungi is achieved by progressive loss of chromosomes throughout cell divisions.

If a polymorphic locus is maintained in finite populations by frequency-dependent selection with selective neutrality at equilibrium, it is generally accompanied by two genetic loads, i.e. the dysmetric and the drift loads. The former arises because the fitness of the population may not be at a maximum at the equilibrium gene frequency and the latter because genetic drift in small populations displaces the gene frequency from its equilibrium value.

In some simple models of frequency-dependent selection considered, the drift load is independent of selection coefficients and is approximately equal to (n−1)/(2Ne), where n is the number of alleles and Ne is the effective population size.

Using four lines derived from a single base population of Lolium perenne by selection for large leaf size (LL), small leaf size (SL), fast rate of leaf appearance (FR), and slow rate of leaf appearance (SR), the inheritance of a number of related characters specifying various aspects of leaf development was studied. F1 and F2 generations were produced for all possible crosses between these four lines.

The genetic differences between the selection lines were largely additive for all characters studied and entirely so for rate of leaf appearance, duration of elongation of a single leaf and for the time interval between the maturation of leaf 3 and the unfolding of the next youngest leaf on the same side of the apex, leaf 5. The non-additive variances noted in rate of total leaf area formation, individual leaf size and its components length and width, and in the rate of leaf elongation, were associated with a tendency towards heterosis in these characters. This was quite marked in some crosses and tended to be larger for the more complex characters, rate of total leaf area formation and leaf size, suggesting that the heterosis was, to a considerable extent, due to interactions between genes controlling component characters.

The data confirmed the earlier finding that the negative correlated selection response between leaf size and rate of leaf appearance was due to a basic association between the maturation of a leaf and the unfolding (onset of rapid elongation) of the next youngest leaf on the same side of the apex. Thus an increase in rate of leaf appearance reduces the duration of elongation of a leaf and this in turn will reduce leaf length. However, the basic association, which seems to be controlled by vascular development of the young leaf, is not entirely invariate.

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.

The frequency of the more common patterns of non-disjunction in Neurospora was studied. Detection of these asci was accomplished by the use of pantothenate requiring strains grown on reduced amounts of pantothenate, so that combinations of dark, pale, and aborted spores provided evidence of non-disjunction. The isolates from five non-disjunction asci were examined in detail and an apparently high frequency of mitotic recombination was detected for presumed disomic isolates. An hypothesis concerning a mechanism of non-disjunction is presented.

Mutants of Ustilago maydis have been isolated both, deficient and derepressed for nitrate reduction. Those deficient in enzyme fall into six groups, one of which is the structural gene. Enzyme which has proved to be more labile than that of wild-type has been isolated from a temperature-sensitive mutant at this locus. All the mutants in the structural gene have xanthine dehydrogenase activity and the situation closely parallels that of Aspergillus nidulans.

The derepressed mutants fall into four complementation groups and all are partially derepressed in that they are further inducible by nitrate. Full derepression can be conferred by induction of a second mutation. In one analysed case the second reinforcing mutation proved to be pheno-typically similar to the first one when separated from it.

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.

Associative overdominance arises at an intrinsically neutral locus through its non-random association with overdominant loci. In finite populations, even if fitness is additive between loci, non-random association will be created by random genetic drift.

The magnitude of such associative overdominance is roughly proportional to the sum of between the neutral and the surrounding over-dominant loci, where is the squared standard linkage deviation, defined between any two loci by the relation

in which p and 1 – p are frequencies of alleles A1 and A2 in the first locus, q and 1 – q are frequencies of alleles B1 and B2 in the second locus, and D is the coefficient of linkage disequilibrium. A theory was developed based on diffusion models which enables us to obtain formulae for under various conditions, and Monte Carlo experiments were performed to check the validity of those formulae.

It was shown that if A1 and A2 are strongly overdominant while B1 and B2 are selectively neutral, we have approximately

provided that 4Nec ≫ 1, where Ne is the effective population size and c is the recombination fraction between the two loci. This approximation formula is also valid between two strongly overdominant as well as weakly overdominant loci, if 4Nec ≫ 1.

The significance of associative overdominance for the maintenance of genetic variability in natural populations was discussed, and it was shown that Nes′, that is, the product between effective population size and the coefficient of associative overdominance, remanis constant with varying Ne, if the total segregational (overdominant) load is kept constant.

The amount of linkage disequilibrium expected due to random drift in experimental populations was also discussed, and it was shown that in the first generation, if it is produced by extracting n chromosomes from a large parental population in which D = 0.

The influence of the linkage group II locus y on DDT resistance in Aedes aegypti has been studied in crosses between the Trinidad resistant strain and QS susceptible strain. The y locus influences DDT resistance in both R/R and R/+ larvae. The effect of y may be interpreted as reducing the penetrance of R (RDDT1), which is also located on linkage group II. y+ is partially dominant and incompletely penetrant in its resistance-enhancing role (although in its pleiotropic effect on larval colour it is dominant and fully penetrant). Penetrance of y+ is influenced by an environmental factor, probably associated with the larval diet.

The effect of y on resistance is evaluated in relation to other genetic influences on the expression of RDDT1.

The significance of polymorphism at the y locus is discussed.

Resistance to mercury has been shown to be associated with the presence of the sex factor (FP) in Pseudomonas aeniginosa. The resistance is expressed in all infected cells even though they do not necessarily function as donors.

For selection of freshly infected recipients when streptomycin or nalidixic acid were used for contra-selection of the donors, the level of mercury had to be reduced to between m/20000 and m/40000 when 500 units of streptomycin were present per ml and to m/40000 when 1·0 mg of nalidixic acid was included in each ml of medium. Normally donor strains would grow in the presence of Hg ions at a concentration of m/2000, which is 10–20 times greater than the concentration in the two selective media.

The kinetics of transfer of the sex factor were investigated and it was shown that transfer began almost as soon as the cells were mixed and was completed in 20 min when 5 min were allowed for pairing.

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.

Twenty-four reciprocal crosses between two green and six chimera cultivars, containing respectively normal green and mutant white plastids in their germ layers, were analysed for their segregation patterns of green, variegated and white embryos, and for their fertility data.

Analysis of variance of fertility data showed that W × G crosses were generally less fertile than the reciprocal G × W crosses, but this was not correlated with selection against any particular class of embryo.

Analysis of segregation patterns showed that they were essentially the same with a constant female and varying male parent, but change the female and the pattern could be radically altered. The six different mutant females with both constant green males could be arranged in a sequence in which white plastids were increasingly successful, and white and variegated embryos increasingly frequent. A similar sequence was demonstrated with three green females and two constant white males. It was concluded that the major control of plastid inheritance was determined by the female nuclear and plastid genotypes, with the male having only a minor, modifying influence even when male plastids were more successfully transmitted than female ones.

The very low frequencies of variegated embryos in some crosses led to a rejection of the classical hypothesis of sorting-out from mixed cells, and its replacement by the hypothesis that pure green or pure white embryos arise by the replication of only one plastid at a time, whereas variegated embryos arise by replication of both plastids.

Seven ascospore colour mutants of the 164 locus of Ascobolus immersus were mapped, and their basic conversion frequencies established. Polarization of the sum of the basic conversion frequencies was observed. The recombination frequencies from the two-point crosses (in repulsion) are nonadditive. The influence of one mutant on the frequency of conversion of another in crosses in repulsion and coupling was pronounced. The frequency of crossing over between a pair of mutants was higher in the cross in repulsion than in coupling. A total of 535 asci containing a pair of wild-type spores were analysed from five crosses in repulsion. 193 6w:2d asci originated from the conversion of the proximal allele, 43 6w:2d asci from conversion of the distal allele and 277 asci exhibited reciprocal recombination. 54 6w:2d asci from one cross in coupling were analysed. These asci were classified and assigned to four classes: proximal allele conversion, distal allele conversion, reciprocal recombination and simultaneous conversion of wild type-alleles to mutants. In all classes of recombinant asci analysed the frequencies of additional exchanges in the adjacent intervals were higher than in random samples of asci. The wild-type chromatid was involved in the additional exchanges in the majority of crosses with a frequency exceeding 60%.

We have recently described a chain-forming mutant of Escherichia coli which showed a decreased resistance to ampicillin and several other antibiotics (Normark, Boman & Mattson, 1969). The gene mediating drug sensitivity was denoted envA and by conjugation mapped at 2–4 min. Transduction experiments have now shown that envA is located between leu and azi at 1·5 min. The mapping was facilitated by the finding that envA mediated sensitivity to actinomycin D, rifampicin and gentian violet. The envA locus could be genetically differentiated from the pea locus mediating resistance to phenethyl alcohol (Yura & Wada, 1968). Studies using partial diploids revealed that envA was recessive to its wild-type allele both when located on an episome and on the chromosome.

Assuming that revertants from envA to the wild-type allele could be selected as ampicillin-resistant derivatives, such mutants were isolated and their phenotype characterized. Reversion to ampicillin resistance was accompanied by reversion to insensitivity to actinomycin D. However, not all revertants exhibited wild-type tolerance to rifampicin. Three different ampicillin-resistant revertants were studied genetically. The results indicate that these strains contain suppressor mutations in the envA region of the chromosome. It is suggested that the envA gene, directly or indirectly, affects the EDTA sensitive ‘permeability barrier’ of the surface layer of Escherichia coli.

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.

Strains of Aspergillus nidulans with, a duplicate chromosome segment are mitotically unstable; in addition to phenotypically improved variants, arising following deletions in either duplicate segment, they give morphologically deteriorated types, some with, enhanced stability. In one isolate, deterioration and increased instability were determined by mutation in a duplicate segment; a more stable derivative no longer had this mutation but had one in another linkage group. Another variant, too unstable for analysis, gave derivatives whose single, new mutations were in different linkage groups. It is proposed that deterioration and increased instability result from tandem duplications on either duplicate segment; transposition of these to non-duplicated regions reduces instability. Another 17 variants had a single new mutation each; mutations, possibly clustered, occurred in all linkage groups. In these strains perhaps transposition preceded analysis. Deteriorated variants gave lineages of types with morphological changes caused by further, superimposed mutations. This continued instability is explained as interaction, in fidelity of replication, of non-homologous chromosome segments.

Instability in A. nidulans stems from chromosome imbalance. As imbalance is known or suspected in other cases of instability it may be possible to show common mechanisms for apparently diverse phenomena.