Hyperhaploid and hyperdiploid colonies of Aspergillus nidulans, disomic or trisomic for one or more chromosomes respectively, are abnormal in phenotype and somatically unstable. It has been shown for Glasgow strains that a different specific phenotype arises, depending upon which chromosome is additional (Pollard, Käfer & Johnston, 1968). This report extends this system and shows that irrespective of the residual genetic background of the isolate, the system of phenotypic specificity applies.

1. In the transduction pro-401 (×) + some of the transductants are surrounded by several hundred small wild-type satellite colonies; these transductants spontaneously release phage which transduces pro-401 to wild-type at high frequency (HFT phage).

2. When the HFT phage is used to infect pro-401 at very low multiplicities of infection, most of the transductants are defective lysogens and segregate proline-requiring phage-sensitive derivatives; these transductants are apparently heterogenotes. At higher multiplicities of infection, or with lysogenic recipients, a higher proportion of satellited transductants is found.

3. The HFT phage preparations transduce only the proline region of the donor genome.

4. The existence is inferred of a defective P22 particle specifically incorporating the proline region of the Salmonella chromosome; these defective particles can establish themselves as prophage and confer immunity upon the infected cell, but are unable to replicate unless a normal prophage is also present. Satellited transductants are lysogenic both for a normal and defective (proline region carrying) phage, and so on lysis release transducing phage.

5. This system is compared with the λdg-gal and P1-dl-lac systems in E. coli.

Using mice that were mosaics for both Xce and phosphoglycerate kinase (Pgk-1) alleles, we have established that the parental source of the Xce gene may affect the probability with which the X chromosome carrying it will remain active. This effect was seen in one allelic combination of Xce but not in another. The relationship between these effects and other phenomena of maternal ‘imprinting’ is discussed.

Maternal inheritance of extranuclear mitochondrial genes has been demonstrated in Aspergillus nidulans using the ‘blue’ ascospore colour mutants in combination with heterokaryon incompatible strains. It appears that heterokaryosis is not a prerequisite of sexual outcrossing, and that recombination of extranuclear mitochondrial markers does not occur in the sexual stage of the cell cycle.

It is widely acknowledged that genetic drift is an important source of variation in response to artificial directional selection. How large should a selection line be in order to reduce the effect of genetic drift to an acceptably low level?

This paper investigates two criteria that can be used to answer this question in relation to short-term response to selection. The first criterion is coefficient of variation of response, and the second criterion is chance of success, where a successful selection programme is one in which the observed response is greater than a certain proportion, β, of expected response.

For a simple mass selection programme with intensity i and heritability h2, the size of population required in order for the coefficient of variation of response to be γ after t generations, is approximately 2/(γih)2t, and the size required for the chance of success to be α after t generations is approximately 2{zα/(β−l)ih}2/t, where zα is the standard normal deviate corresponding to the probability α.

As an example, suppose it is required that after t generations the coefficient of variation of response be 10% or that there be a 90% chance of achieving at least 9/10 of expected response. Since ih ≤ 2 in most selection programmes, the size of population required is at least 50/t or 82/t respectively. If ih ≤ 1, the corresponding sizes are 200/t and 328/t.

Results are extended to enable the calculation of size of population required for any type of artificial directional selection programme, including those in which generations overlap.

Eighteen mutations of Saccharomyces cerevisiae, at eight loci, isolated as antisuppressors of SUPQ2, an ochre-suppressing allele of SUP11, were crossed with three other suppressors.

They were found to abolish the ability of SUP2 (inserting tyrosine), to suppress the ochre mutations ade2.1 and can1.100, but not its ability, to suppress his5.2 or lys1.1. When coupled with any antisuppressor, SUPQ5, inserting serine, was also unable to suppress ade2.1, but the suppression of other ochre mutations varied from one asu-SUPQ5 strain to another. No antisuppressor affected the ability of SUP11-am, an amber-suppressing allele of SUP11, to suppress trp1.1, an amber mutation.

The usual systems of assay using techniques of chromosome substitution demonstrated in Drosophila and wheat are not applicable to barley (Hordeum vulgare). Chromosomal material for assay may, however, be substituted from one variety into another by using translocations to mark and restrict crossing over in the chromosomes to be transferred. This paper describes the isolation and assay of lines derived in this way.

Seven substitution lines derived from the donor variety Maris Badger and the recipient variety Mars have been scored for quantitative characters in two field trials.

The results indicate that variation in flowering time and other associated characters is largely determined by genes on chromosome 2 and that chromosome 4 is involved in the control of plant height.

The feasibility of the technique as a method of assaying the contributions of chromosomes to qualitative characters by substitution in a diploid is discussed.

Evolutionary consequences of natural selection, migration, genotype–environment interaction, and random genetic drift on interpopulation variation and covariation of quantitative characters are analysed in terms of a selection model that partitions natural selection into directional and stabilizing components. Without migration, interpopulation variation and covariation depend mainly on the pattern and intensities of selection among populations and the harmonic mean of effective population sizes. Both transient and equilibrium covariance structures are formulated with suitable approximations. Migration reduces the differentiation among populations, but its effect is less with genotype–environment interaction. In some special cases of genotype–environment interaction, the equilibrium interpopulation variation and covariation is independent of migration.

FP transfer to recombinant and non-recombinant recipients of Pseudomonas aeruginosa strain I has been investigated under controlled conditions. When transferred to recombinants, the sex factor appeared to enter first and did not seem to be linked to the early chromosome markers. Five to twenty percent of the recipient population were found to be FP+, depending on the time allowed for pairing. Only 40% of the recombinants were FP+ at 90 min. A possible relationship between FP and chromosome has been discussed.

Postmeiotic segregation (PMS) of genetic variants occurs when a DNA heteroduplex formed during meiotic recombination goes undetected by repair enzymes and is transmitted unresolved to the meiotic products. PMS provides an alternative explanation for the origin of mosaics now attributed to half-chromatid mutation. In multicellular diploid eukaryotes, PMS could result in mosaic individuals with unusual migration patterns for proteins studied by gel electrophoresis. If the gonade were mosaic, complex progenies containing as many as six phenotypic classes at a single locus could be produced.

Identity disequilibrium, ID, is the difference between joint identity by descent and the product of the separate probabilities of identity by descent for two loci. The effects of ID on the additive by additive (a * a) epistatic variance and joint dominance component between populations and in the additive, dominance and a * a variance within populations, including the effects on covariances of relatives within populations, were studied for finite monoecious populations. The effects are formulated in terms of three additive partitions, ηb, ηa and ηd of the total ID, each of which increases from zero to a maximum at some generation dependent upon linkage and population size and decreases thereafter. ηd is about four times the magnitude of the other two but none is of any consequence except for tight linkage and very small populations. For single-generation bottleneck populations only d is not zero. With random mating of expanded populations ηb remains constant and ηa and ηd go to zero at a rate dependent upon linkage, very fast with free recombination. The contributions of joint dominance to the genetic components of variance within and between populations are entirely a function of the η's while those of a * a variance to the components are functions mainly of the coancestry coefficient and only modified by the η's. The contributions of both to the covariances of half-sibs, full-sibs and parent-offspring follow the pattern expected from their contributions to the genetic components of variance within populations except for minor terms which most likely are of little importance.

1. Inactivation of one X chromosome in somatic cells of female mammals is a form of dosage compensation of sex-linked genes, but the mechanism is entirely different from that operating in Drosophila. The latter is designated as dosage compensation sensu strictu.

2. There is no dosage compensation of barred, sex-linked dilution or slow-feathering in domestic fowls, of almond or faded in pigeons, or of cinnamon in canaries. Among Lepidoptera the same is true of sex-linked melanism in Lymantria monacha and of a locus controlling haemolymph colour in Choritoneura spp. There is no positive evidence that dosage compensation occurs outside Drosophila and mammals.

3. Sex-chromatin in female birds (heterogametic) has been reported by several authors; the genetical evidence is against the possibility that this represents (as in mammals) an inactivated X chromosome. Sex-chromatin in the heterogametic sex also occurs in some (not all) Lepidoptera and Heteroptera; in Heteroptera it usually represents a heteropyknotic Y chromosome.

4. Some complications in Muller's theory of dosage compensation sensu strictu are discussed. Not all ‘compensatory modifiers’ are necessarily sex-linked.

5. The problem of dosage compensation in species with impaternate males is discussed; fused in Habrobracon is not compensated.

A method for obtaining linear estimates of heritability and genetic correlation is given. It is based, essentially, on selecting, from a pedigreed population, prospective parents for which estimates of average genotype and phenotype values are obtained; a regression of genotype on phenotype value is then determined from a straight line fitted through points representing the population mean genotype and phenotype on one hand and the mean genotype and phenotype of selected parents on the other.

The method permits an evaluation of asymmetry in response for a trait selected in both directions, as well as asymmetry in correlated response to selection of two different traits, with data from a single pedigreed population.