The shapes of T1 and T2 vertebrae from unselected Q strain mice and from strains selected for large and small body size were studied by Fourier analysis in order to ascertain whether shape change was produced by size selection. The vertebrae of large, small and control strains were easily distinguishable, but between replicate groups shape differences were less marked. The main component of shape change was size related, but mice unselected for size also showed a non-size-related shape change.

By application of the neutral model of phenotypic evolution, quantitative estimates of the rate of input of genetic variance by polygenic mutation can be extracted from divergence experiments as well as from the response of an inbred base population to selection. The analytical methods are illustrated through a survey of data on a diversity of organisms including Drosophila, Tribolium, mice, and several crop species. The mutational rate of introduction of genetic variance (Vm) scaled by the environmental variance (VE) is shown to vary between populations, species, and characters with a range of approximately 10−4 to 5 × 10−2. Vm/VE for Drosophila viability is somewhat below this range, while hybrid dysgenesis may temporarily inflate Vm/VE beyond 10−1. Potential sources of bias and error in the estimation of Vm are discussed, as are the practical implications of the observed limits to Vm/VE for projecting the long-term response to selection and for testing adaptational hypotheses.

Variance components of fitness under the stabilizing selection scheme of Wright (1935) for metric characters are calculated, extending his original analysis to the case with any number of alleles and multiple characters assuming additivity of gene effects. They are calculated in terms of the moments of the effects of alleles at individual loci for the metric characters. From these formulas, the variance components of fitness are evaluated at the mutation–selection equilibria predicted by the ‘Gaussian’ approximation (Lande, 1976), which is applicable if the per locus mutation rate is high, and the ‘House of Cards’ approximation (Turelli, 1984), which is applicable if the per locus mutation rate is low. It is found that the additive variance of fitness is small compared to non-additive variance in the ‘Gaussian’ case, whereas the additive variance is larger than non-additive variance in the ‘House of Cards’ case if the number of loci per character and the number of characters affected by each locus are not too large. With the assumption that a significant portion of fitness is due to this type of stabilizing selection, it is suggested that the real parameters are in the range where the ‘House of Cards’ approximation is applicable, since available data on variance components of fitness components in Drosophila show that the additive variance is far larger than the non-additive variance. It is noted that the present method does not discriminate the two approximations if the average values of the metric characters deviate from the optimum values. Other limitations of the present method are also discussed.

Dysgenic and non-dysgenic base populations were made by reciprocal crossing of Harwich (P) and Canton-S (M) strains. From each cross, two up and two down selection lines were established, with selection on abdominal bristle number for ten generations. The intensity of selection was 10 out of 50 individuals from each sex. Mean bristle number, phenotypic variation and heritabilities were compared between dysgenic and non-dysgenic populations under selection. Except for an anomalous non-dysgenic downline in which a mutation of large effect occurred, all lines showed similar responses to selection. These results contrast with the results reported by Mackay (1984, 1985) in which substantial increases were obtained for response to selection, phenotypic variation and heritability in the dysgenic compared to non-dysgenic lines. There are some indications that the higher response in our aberrant non-dysgenic downline is the result of transposition. Possible explanations for the occurrence of transposition and dysgenesis in the lines derived from nondysgenic crosses are discussed.

The amount of linkage of disequilibrium maintained in a two-locus infinite population model by gene conversion and recombination is examined. Intrachromosomal conversion (conversion between different loci on the same chromosome) generates positive linkage disequilibrium. Specifically, = p(1 − p) [1 − r/(γ + r − γr)], where p is the frequency of allele A at both loci, r is the recombination rate between loci and γ is the per-gamete conversion rate. Somewhat unexpectedly, interchromosomal conversion (conversion between loci on different chromosomes) also generates positive disequilibrium, albeit very small. More interestingly, the behaviour of this disequilibrium as a function of recombination is unusual. If β is the interchromosomal conversion rate between a pair of loci, then = p(1 − p) [rβ/(β+r − βr)]. increases with increasing recombination, being zero for the case of complete linkage (r = 0), and maximized at r = 1/2. This unusual behaviour can be accounted for by the generation of excess coupling gametes when an interchromosomal conversion event is followed by recombination.

The sex-reversal mutation, Sxr and a variant form, Sxr′ have been established on the inbred C57BL/6Mcl background by repeated backcrossing to form the CB and CB′ strains, respectively. DNAs of normal XY, XX Sxr and XX Sxr′ as well as XY Sxr and XY Sxr′ carrier male mice have been digested with the restriction enzymes Hae III and Hinf I and electrophoresed. The DNAs show many common but also differing hybridization bands with synthetic oligonucleotide probes. In XY Sxr (and XY Sxr′) carrier males, the hybridization patterns of normal XY and those of XX Sxr (and XX Sxr′) males are simply superimposed. Individual differing bands can be categorized by their differential hybridization behaviour to the (GATA)4, (GACA)4, (GATA)2 GACA (GATA)2 and (GATA)3 (GACA)2 probes. In general, the hybridization patterns are regularly inherited. In addition to the predominant pattern in each strain, one additional XX Sxr and one additional XX Sxr′ hybridization pattern was observed: the additional pattern in the CB strain was transmitted (via variant XY Sxr carriers) while the secondary XX Sxr′ pattern in the CB′ strain could only be observed once. Thus ‘DNA finger printing’ with oligonucleotide probes can successfully be used to discriminate the DNAs of normal Y chromosomes, XX Sxr and XX Sxr′ variants as well as XY Sxr and XY Sxr′ carrier mice. Implications of the comparatively high unequal recombination rate involving the murine Y chromosome are discussed, as well as possible mechanisms.

We have analysed data on weight and tarsus length collected during a long-term study of natural populations of Great Tits to evaluate the relative importance of genetic variation in body size. Some of our data were collected over a 25-year period, and therefore include a relatively large sample of naturally occurring environmental conditions. An overall heritability estimate calculated from the uncorrected mean weights of breeding birds amounts to 0·5. This estimate is unlikely to be influenced by resemblance in environmental conditions between relatives. Heritability estimates based on the size of fledglings vary between zero and the value for adults, depending on the environmental conditions during growth. If the feeding conditions for the nestlings are poor, no resemblance between parents and offspring is observed. Selection against small nestlings acts strongly on the environmental variance. This is concluded from the higher heritability estimates in the same cohorts after survival for at least three months after fledging, compared to measurements on nestlings. Such selection acting differentially on the genetic and environmental components of the phenotypic variance has important consequences for our ability to make predictions of phenotypic change from measured natural selection. Nevertheless, the amount of genetic variation would allow rapid response should selection on adult size occur.

A polygenic model has been simulated in order to reveal the process whereby selection in an infinite population can lead to an increase in the frequency of alleles causing higher rates of recombination (CH alleles). Directional selection generates repulsion linkage disequilibrium (+ − + −), which is less strong in CH gametes (gametes carrying CH alleles). In consequence, CH gametes contribute greater phenotypic variability, and therefore respond more to directional selection: that is, they accumulate more selectively favoured alleles. CH alleles then increase in frequency by hitch-hiking. In contrast, normalizing selection, or frequent changes in the direction of selection, favour alleles for a low recombination rate.

Genet. Res., Camb. (1988) 51. Facing page 1.

The photograph of Douglas S. Falconer should have been dated December 1987 and credited to

ANTONIA REEVE PHOTOGRAPHY

The normal response to injection of noradrenaline (NA) in newborn lambs is an increase in metabolic rate and rectal temperature, due to the stimulation of non-shivering thermogenesis. In a previous study 6 out of 7 lambs born to a sire previously selected for low resistance to cold failed to show this characteristic response and were termed non-responders. The sire, 2 of his male offspring and 6 sires selected randomly from the flock were mated to several ewes and the response to NA stimulation recorded in 116 newborn lambs. Control sires produced only normal responder lambs whereas the remaining sires all produced both responder and non-responder lambs. The proportion of non-responders was not significantly different from 0·50, which is consistent with a dominant major gene. Analysis of the quantitative traits, peak metabolic rate and peak rectal temperature following NA injection confirms that a major gene is segregating in the study population, but is unable to distinguish between dominant and recessive modes of inheritance. Absence of non-responders in other studies suggests that dominance is more likely. This new genetic resource could aid our understanding of brown adipose tissue metabolism and the effect of catecholamines on metabolic pathways.

We constructed a cloning vector (pMT603) based on the low copy number plasmid SCP2*. pMT6O3 is unstable because it lacks the SCP2* stability region and carries the selectable marker thiostrepton-resistance and a tyrosinase gene which results in melanin production. This allows easy testing of plasmid stability and we demonstrated its usefulness by cloning a plasmid stability function.