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1. Selection for long or short wings was carried out in three pairs of lines of which two were started from the same basic population. At the end of the selection experiment the frequencies of the chromosomal arrangements were determined in each line and compared with the corresponding original frequencies to see if the chromosomal polymorphism of Drosophila subobscura is related to the genetic variation of size in a regular way.
2. The three pairs of lines show an asymmetrical response to selection. Selection for long wings is less effective in changing the mean of the population than selection for short wings.
3. Heritability is lower in the lines selected for long wings, especially in the later generations of selection.
4. Viability shows a very small decrease during selection in most selected lines.
5. In no case does the coefficient of variability show statistically significant changes, but there is a general tendency for it to decrease.
6. Selection for long wings favours combinations heterozygous for the standard chromosome orders and specific complex inversion orders. Selection for short wings generally fixes in homozygous combination specific complex inversion orders.
7. The heterozygous combinations of the standard chromosomal orders, which are most frequent in northern populations, when combined with the complex inversion orders which are most frequent in southern populations, have a heterotic effect on size.
8. The complex inversion orders usually fixed in homozygous combinations in the lines selected for short wings are those most frequent in southern populations which have a smaller mean size than northern populations.
9. The blocks of genes integrated in ‘supergenes’ in the inverted segments of the chromosomes of D. subobscura differ in genetic composition with respect to the control of wing length.
The frequency of cotransduction of motC and H1 in Salmonella has been investigated, using four Salmonella serotypes and many serotypic recombinants as donors and S. typhimurium motC mutant as recipient. The frequency varied with the four serotypes from 7% to 52%. It is suggested that the difference in frequency arises from not only differences in genetic homology between the chromosome of the recipient and the fragment from the donor, but also from differences in genetic composition of the chromosome fragments carried by the phage. The frequency of serotypic recombinants selected for motC+ and H1 gene of the donor is generally higher than with recombinants selected for flaK+ and H1. The difference in genetic homology between S. typhimurium and other species is more marked in the region between H1 aud flaK than between motC and H1.
The sequence of development of salivary gland chromosome puffs in Drosophila melanogaster cultured on live yeast and RNA-deficient medium has been studied in late larval and prepupal stages. Differences in puffing pattern between individuals cultured in the two environments are almost entirely due to shifts in the relative timing of puff development at specific chromosome sites. Detailed studies on the right arm of the second chromosome indicate that, at certain sites, puffing activity spreads to adjacent lettered subdivisions of the chromosome. There are differences in the extent of lateral spreading of activity into adjacent regions in the two environments which may be due to clustering of functionally related genes.
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.
A new mutation, Sleek, similar in appearance to mutations at the Ta, cr and dl loci, has been investigated. It is inherited as an autosomal dominant and maps very close to dl on chromosome 13. Allelism with dl seems probable since Sleek interacts with dl but not with cr. The unusual occurrence of dominant and recessive alleles at the same locus which produce a similar mutant phenotype suggests that the locus might either code for a multimeric protein or a regulatory product.
The accumulation of beneficial and harmful mutations in a genome is studied by using analytical methods as well as computer simulation for different modes of reproduction. The modes of reproduction examined are biparental (bisexual, hermaphroditic), uniparental (selfing, automictic, asexual) and mixed (partial selfing, mixture of hermaphroditism and parthenogenesis). It is shown that the rates of accumulation of both beneficial and harmful mutations with weak selection depend on the within-population variance of the number of mutant genes per genome. Analytical formulae for this variance are derived for neutral mutant genes for hermaphroditic, selfing and asexual populations; the neutral variance is largest in a selfing population and smallest in an asexual population. Directional selection reduces the population variance in most cases, whereas recombination partially restores the reduced variance. Therefore, biparental organisms accumulate beneficial mutations at the highest rate and harmful mutations at the lowest rate. Selfing organisms are intermediate between biparental and asexual organisms. Even a limited amount of outcrossing in largely selfing and parthenogenetic organisms markedly affects the accumulation rates. The accumulation of mutations is likely to affect the mean population fitness only in long-term evolution.
The origin of triploid (3N) 5½-day blastocysts in rabbits is inferred from the segregation of sex chromosomes and of an autosomal M-marker whose properties are described. 39 triploids and no tetraploids were scored among 1454 chromosomally scored blastocysts. A delay of 8 h between an ovulatory injection and subsequent insemination raised the estimated normal incidence of 0·59% triploid blastocysts to 3·13%. The increase is ascribed primarily to digyny (17 blastocysts), and to diandry probably mediated by dispermy (1 blastocyst). The triploid components of the two 2N/3N mosaics and the one 3N/6N were digynic. Neither superovulation nor insemination of excessive numbers of spermatozoa could be shown to give rise to triploid embryos. The diandric triploid was X Y Y, the first of this constitution apparently reported in the rabbit. There was some evidence that X X Y triploid blastocysts up to 5½-day gestation are more viable than X X X. In the 2N/3N mosaics each component had been entered by one spermatozoon, and the dliploid component could not have been merely a contamination by dliploid maternal somatic cells. In 2N/4N, 2N/4N/8N and 3N/6N mosaics, each polyploid component showed an exact doubling of the marker chromosome constitution of a component of lower ploidy; their origin is ascribed to doubling or redoubling of chromosome number in isolated embryonic cells. With earlier data included, 49·08 (± s.e. 1·96)% of 652 diploid blastocysts were X Y. 460 non-experimental weaned rabbits were all cliploid.
The chromosomal region surrounding the ed, dp and cl genes has been studied cytogenetically (24–26 on 2L chromosome). It contains three Minutes and a haplo-sterile function. For isolation of deficiencies and mutations these haplo-insufficient functions were covered by an insertional translocation of 24D4-25F2 into the X chromosome, or by tandem duplications. 112 lethal and visible mutations induced by EMS and X-rays have been localized by deficiency mapping to 20 subregions. They specify 42 loci in a 48 band interval consistent with the notion that most of the bands encode a single lethal function. The dp, DTS, tkv and suppressor/enhancer loci for position-effect variegation were studied in detail. A dominant suppressor function was localized within the structural part of the dp complex. New non-conditional lethals have been isolated for the DTS locus. Complementation analysis with the previously identified dominant heat-sensitive alleles places the site for heat sensitivity in the middle of the locus. Two haplo-abnormal enhancers of position-effect variegation were localized in the region 25F2–26A1. A triplo-abnormal suppressor function maps to 26B2–5; 26B9. The dose-dependent functions of these loci were studied by the use of deficiencies and duplications.
The American raspberry variety Chief is shown to carry three dominant genes, A5, A6 and A7, each capable of conferring strong resistance to Amphorophora rubi strain 1.
Chief also carries three genes, A2, A3 and A4, for resistance to A. rubi strain 2. A2 is a dominant gene conferring full resistance by itself; A3 and A4 are dominant complementaries, neither gene by itself having any effect on resistance. A5 is linked with either A3 or A4 with a crossover value of 10%.
The gene A1 from Baumforth A, which confers resistance to strains 1 and 3, when combined with A3 gives resistance to strain 2 also. Thus the three strains of A. rubi at present recognized on raspberries in Britain can be controlled by using either the combination A1A2 or A1A3.
In the homozygous condition, the mutation adr (arrested development of righting response) of the mouse causes a myotonia and a drastic reduction of the Ca2+-binding protein parvalbumin (PV) in fast muscles. Using a rat PV probe, a mouse cDNA clone was isolated from a λgt11 wild-type fast-muscle library and its nucleotide sequence was determined. The protein coding and the 3′ non-translated regions of the mouse gene show extensive homology with the rat PV gene. The result of Southern blot hybridization is consistent with a single copy gene for parvalbumin. Restriction fragment length polymorphisms (RFLPs) between Mus musculus domesticus (e.g. C57BL/6) and Mus spretus (SPE) were detected with the enzymes Eco RI, Pst I, and Sst I. The restriction fragment patterns of DNA samples from 65 individual offspring of (C57BL/6 × SPE)F1 × C57BL/6 backcrosses were tested with the PV probe and matched, for linkage detection, to pre-existing patterns established with various RFLP probes on the same samples. A co-distribution of PV-RFLPs with Pvt-1 and Mlvi-2, which had been localized on chromosome 15, was detected. Thus, the structural gene for PV, designated Pva, maps to chromosome 15 of the mouse whereas the adr mutation shows no linkage with markers on this chromosome. Gene locus homology between chromsome 15 of the mouse and chromosome 22 of man (which carries the human PV gene) is discussed.
The effect of the P-M system of hybrid dysgenesis in Drosophila melanogaster on unequal crossing-over was studied using the Bar duplication. This system of dysgenesis had no demonstrable effect on the rate of Bar reversion. In the course of the study it was found that there was a greatly reduced rate of reversion in two homozygous inversion stocks. Further, one revertant was found which may result from unequal crossing over at the Bar locus in males.
With 12 alleles at the Est-α locus of Drosophila virilis, 44 genotypes of females heterozygous for a pair of them were constructed, and about 4 × 104 of their F1 progenies per genotype were electrophoretically examined. Eighty-three variants different from both of their parental alleles were obtained from a total of 2·0 × 106 progenies. Statistical analysis suggested most of their variants to be recombinants. And no null or inactive allele, of which frequency is several percent in natural populations, appeared in 11·6 × 104 progenies from females heterozygous for active alleles. These results suggest that the high variation of the Est-α locus in this species is generated by recombinants from female heterozygotes.