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The hordein polypeptide controlled by the Hrd G (Hor 4) locus in Elgina and derived lines was purified by preparative isoelectric focusing. The amino acid composition was similar to those of the major B hordeins encoded by the Hor 2 locus. Genetic analysis confirmed that Hor 4 is located proximally to Hor 1 on the short arm of chromosome 5. It is speculated that Hor 4 arose by translocation of genes from Hor 2, possibly in an ancestor of Elgina.
A mathematical method for evaluating the probability that a locus is monomorphic for the same allele in related species is developed under the neutral mutation hypothesis. A formula for the proportion of identically monomorphic loci in related species is also worked out. The results of the application of this method to Drosophila data do not support Prakash & Lewontin's (1968) contention that the strong association between gene arrangements (inversion chromosomes) and alleles at protein loci is evidence of coadaptation of genes in the inverted segment of chromosomes. Similarly, unlike Haigh & Maynard Smith's (1972) contention, the monomorphism of the haemoglobin α chain locus in man can be accommodated with the neutral mutation hypothesis without invoking the bottleneck effect.
From the F2 ratios of crosses between Drosophila melanogaster strains homozygous for the AdhF(F) and the Adhs(S) allele it has been concluded that the developmental time of FF homozygotes is shorter than that of SS homozygotes. This difference is found to be reinforced by increasing levels of crowding. A further analysis of developmental times has been performed by the transfer of larvae to agar medium after they have stayed for periods of variable length on regular food. From the percentage of emerging adults it can be concluded that FF larvae and, to a lesser extent FS larvae, either reach their critical weights for pupation earlier than SS larvae or possess a lower critical weight. These differences in developmental time influence the course of allele frequencies. Between populations kept on a 2-week transfer schedule and on a 3-week schedule a divergence of allele frequencies is observed, in the former a decrease in S frequency occurs. The relevance of the observed differences in developmental time for the maintenance of the Adh polymorphism is discussed for laboratory populations kept on regular food and at varying densities.
We have determined the map position of the gene encoding a common precursor protein for diapause hormone and pheromone biosynthesis-activating neuropeptide (the DH-PBAN gene, Dh)in the silkmoth, Bombyx mori. First we compared the structure of introns in the DH-PBAN gene by the polymerase chain reaction, and found that the Dh locus carried three alleles, DhA1, DhA2 and DhB. The DhA1 and DhA2 alleles contained a fourth intron consisting of 740 bp, whereas DhB had a longer fourth intron of 770 bp. DhA1 and DhA2 contained a fifth intron consisting of 940 bp, whereas the fifth intron in DhB was much longer and consisted of 1700 bp. DhA1 was distinguished from DhA2 by an RFLP in the fifth intron after digestion with Rsa I. Linkage analyses using these polymorphisms showed that Dh was linked to the bp gene on chromosome 11, and independent of markers on chromosomes 1, 2, 3, 4, 5, 6, 7 and 13. To determine the map position, we obtained F1 hybrids between the n501 strain (K DhA1) and the w30 strain ( + KDhB), and backcrossed the F1 hybrid to females of the w30 strain. From the segregation of K and Dh in 864 individuals in the next generation, the recombination value was calculated as 25·5 % between K and Dh. Similarly we obtained backcross progeny between the No. 744 strain (BuDhA1) and the w30 strain ( + BuDhB), and calculated the recombination value between Bu and Dh as 30·4% from 487 progeny. Because k and Bu had already been mapped at positions 11–23·2 cM and 11–28·7 cM, respectively, we mapped Dh at 11--2·2 cM. The Dh locus is different from any loci which are known to control diapause, development or growth.
Mice gaining 3 or more standard deviations above the mean were noted beginning in generation 25 in a line selected for high 21–42 day weight gain. The exceptional growth rate appears to be due to an autosomal recessive gene, based on the following: (1) the exceptional individuals appeared suddenly, in only one of 2 closely related sublines; (2) mating high growth individuals to unrelated, normal size strains produces relatively uniform F1's with mean gains below the mid-parent average; (3) F2's have a distribution markedly skewed towards high gain and a coefficient of variation approximately double that of F1's; (4) true breeding high growth strains can be established in one generation by intermating the largest F2's; (5) intermating normal F2's produces progenies with a distribution similar to the F1 except for a few large segregates; (6) high growth segregates have been obtained in F2's from each of 4 successive backcrosses to the C57BL/6 inbred line. The symbol hg (high growth) is proposed for the postulated gene, which appears to be completely recessive. Frequency of positively identified segregates in F2's and backcrosses is on average less than 25 and 50%, due probably to some overlap of Hg- and hghg distributions. Gain of hghg individuals from 21–42 days is 30–50% higher than of Hg- contemporaries; mature weight is also much higher, while 21-day weight of hghg individuals in segregating litters is slightly lower. Fertility of homozygotes ranges from normal to as much as 40% lower than for comparable Hg- mice; hghg mice are not obese. The gene may provide a useful model for study of regulation of mammalian growth.
Cells carrying traJ− mutants of F are transfer-deficient and are good recipients in conjugation (Achtman, Willets & Clark, 1972). In addition, the traJ gene product is involved in pilus- and in plasmid-specificity (Willetts, 1971). J-independent mutants were isolated as revertants of a traJ− mutant; they still carry the traJ− mutation but also carry at least one other mutation which results in transfer in the absence of the traJ gene product. J-independent transfer of these mutants is not inhibited by the R 100 repressor. Various models are presented which can account for the properties of traJ− mutants and of these J-independent revertants.
Segregation Distorter (SD) chromosomes are preferentially recovered from SD/SD+ males due to the dysfunction of sperm bearing the SD+ chromosome. The proportion of offspring bearing the SD chromosome is given the symbol k. The nature of the frequency distribution of k was examined by comparing observed k distributions produced by six different SD chromosomes, each with a different mean, with k distributions predicted by two different statistical models. The first model was one where the k of all males with a given SD chromosome were considered to be equal prior to the determination of those gametes which produce viable zygotes. In this model the only source of variation of k would be binomial sampling. The results rigorously demonstrated for the first time that the observed k distributions did not fit the prediction that the only source of variation was binomial sampling. The next model tested was that the prior distribution of segregation ratios conformed to a beta distribution, such that the distribution of k would be a beta-binomial distribution. The predicted distributions of this model did not differ significantly from the observed distributions of k in five of the six cases examined. The sixth case probably failed to fit a beta-binomial distribution due to a major segregating modifier. The demonstration that the prior distribution of segregation ratios of SD lines can generally be approximated with a beta distribution is crucial for the biometrical analysis of segregation distortion.
Analysis of a series of exceptional ry+ half-tetrads, produced in mass matings involving rosy mutant heterozygous half-tetrads, provides rigorous demonstration of the occurrence of non-reciprocal as well as reciprocal recombination events within the rosy cistron of Drosophila melanogaster. Inferences about allele recombination drawn from this and other studies in Drosophila provide a strong argument that gene conversion occurs as a regular event in higher eukaryotes.
Certain drd mutants of fi+ R factors, when carried by strain HfrC, allowed polarized transfer of the Hfr chromosome to occur at the normal rate. These mutants were independently shown to be repressor-sensitive and so owed their de-repression to failure to produce represser (i−). With other drd mutants, independently shown to be repressor-insensitive (0c), the rate of polarized chromosome transfer was as low as with the wild type and only R pili were produced by the HfrC+ bacteria. These R factors, therefore, continued to produce repressor and the donor behaviour of an Hfr strain depends on functioning of the integrated F.
A simulation study was undertaken of methods of subdividing populations into several small sublines and utilizing the variances generated between lines by selecting among them. Crosses of chosen lines were made, and either selection was continued in a single large population (single cycle) or the population was subdivided again (repeated cycles). As a control for the efficiency of these schemes, a single large population was maintained and selected at the same intensity from the outset. Simple models were used of additive or completely dominant genes, usually of equal effect and equally spaced on a single chromosome.
The single and repeated cycle structures give similar results, but the repeated cycle structure is more extreme.
With additive models intense selection between lines gives short-term advances, but causes a reduction in the limit when compared with a single population. The effect on the limit is greatest with free recombination, very small with complete linkage. If no selection is practised between lines the limit is unaffected, but takes longer to attain.
With complete dominance, and the recessive allele initially at low frequency, greater responses from selection are obtained within sublines than in the large population, large gains are made from selection between sublines, and a higher limit can be reached. If the recessive allele is at high initial frequency the subdivision is not beneficial.
Some simple theory is developed to explain these results. It is concluded that subdivision and crossing schemes are unlikely to be very useful except for elimination of deleterious recessive genes.
When DNA sequence data on various kinds of homologous genes sampled from two related species are available, there is a way to infer the effective size of their ancestral species, which is a simple consequence of gene genealogical considerations. This method, when applied to the common ancestral species of human and rat, human and mouse, human and bovine, or rodents and bovine estimates their effective sizes all to be of the order of 107, supporting the view that these species indeed shared, around 75 million years ago, a common ancestral species from which they are descended. The effective size thus estimated would imply that the ancestral species was abundant enough to have ample opportunity for adaptive radiation. The extent of silent polymorphism in that species might have been very large, possibly comparable to the number of silent substitutions accumulated in a gene after the mammalian divergence. Some causes that may alter these results and require a more elaborated statistical analysis are discussed.