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The accumulation of selfish DNA in eukaryotic genomes was studied from the standpoint of population genetics. Selfish DNA is assumed to replicate itself within a haploid set. For the selectively neutral case, the fate of a single self-replicating DNA segment (unit) within a population was investigated by the method of the probability generating function, and by Monte Carlo simulation, with special reference to the probability of survival and average number of units per haploid set. For the selectively deleterious case at the organismal level, the equilibrium between new occurrence and selective elimination was studied, and the average and variance of the number of units per haploid set in the population was examined by Monte Carlo simulation. It is shown that the process of self-replication (duplication–deletion) plays an essential role for the maintenance and elimination of selfish DNA.
A genetic analysis was made of the Female-lethal (Fl) locus of Drosophila melanogaster. This is an X-linked mutation which causes lethality only in females. Other alleles do not complement Fl and are either lethal or sterile when homozygous in females. Complementation studies on Fl alleles demonstrate that there is no simple ranking of these alleles in terms of severity of phenotypic effect. Dosage manipulation of Fl alleles indicates that the sex-specificity is not a consequence of gene dosage effects. Viability studies on males carrying Fl alleles show that Fl alleles have no effect on viability regardless of the presence or absence of a Y chromosome. The Fl locus is therefore sex-specific. The hypothesis that Fl+ is involved in the establishment of imaginal phenotypic sex cannot be substantiated on the basis of experiments utilizing sex-change mutations.
The advantage in using membrane filters for crosses between P+ (donor) and P− (recipient) strains of Vibrio cholerae (Bhaskaran, 1964; Bhaskaran, Sinha & Iyer, 1967) is probably due to more frequent and effective contacts between the cells on the surface of the membrane than is possible in fluid media with actively motile cells of this species. The transfer of the fertility (P) factor itself, as well as the yield of genetic recombinants, was considerably improved by this procedure.
Twelve isogenic X chromosome lines from a single natural population of Drosophila melanogaster were tested for their potential to induce gonadal dysgenesis and singed-weak mutability in P-M hybrid dysgenesis. The correlation between sterility and mutability was significantly positive for Cross A, confirming the results reported by Engels (1984) and Kocur, Drier & Simmons (1986). In Cross A* cytotype tests, however, two of the lines gave strikingly different results when measured by the gonadal dysgenesis test as compared to the singed-weak test. Positive correlations between traits within a given line were generally not observed. The results suggest that the relationship between gonadal dysgenesis production and the mobilization of P elements in singed-weak mutability is more complicated than that proposed by Engels (1984). The two phenomena may be separable under certain conditions. Neither test can be taken as an adequate characterization of the hybrid dysgenesis ‘profile’ of a line of flies.
It has long been believed that partially paired chromosomes observed at early meiotic prophase represent synapsis caught in the act and that crossing over must follow or accompany this stage. In contradiction to this it has often been suggested that certain observations (e.g. the occurrence of 3: 1 ratios from individual tetrads of yeast, Neurospora and Aspergillus) are most easily explained if it is assumed that crossing over occurs at the time of reduplication which in turn is now thought to occur during the premeiotic interphase (Taylor, 1957). Another phenomenon, which has been reported in Neurospora, Drosophila and bacteriophage, and apparently must be fitted into any successful model of recombination, is localized negative interference.
The first mutation step towards ampicillin resistance in Escherichia coli occurs in the ampA gene, and gives resistance to a D, L-ampicillin concentration of 10 μg/ml. Using interrupted conjugation and transduction experiments ampA was found to be located at 82 min on the time scale of Taylor & Thoman (1964). A number of adjacent markers were studied and the probable gene order of the ampA region was found to be argH-metA-uvrA-ampA-purA-fdp-pyrB. Two independent alleles of ampA were cotransduced with fdp+ and purA+. The phenotypic expression of ampA in a purA strain has been investigated.
Among temperature-sensitive mutants of Escherichia coli a strain was discovered requiring D-alanine for growth. It was proved to possess an altered alanine racemase. The structural gene for this enzyme, designated alr, is located between metB and pur A. The properties of the enzyme and its locus suggest that it is not under control of the mechanisms which regulate mucopeptide formation. A suppressor of the alr mutation was discovered near trp, and termed msuA.
Two male-sterile chromosome anomalies, the insertion Is(7; 1)40H and the tertiary trisomy, Ts(512)31H, were found to be associated with reduced ovarian volumes in immature females. Together with the reciprocal translocation, T(11; 19)42H, in which this effect was described previously, reduced ovaries have been found in all three male-sterile chromosome anomalies investigated so far, suggesting that ovarian involvement is likely to be common in these conditions. Assuming that the smaller ovarian size reflects a reduction in the number of oocytes, it is suggested that male-sterile chromosome anomalies may exert basically similar deleterious effects on meiotic germ cells in males and females, the difference in outcome being due to cell-physiological differences between spermatocytes and oocytes and to the small number of surviving oocytes required for fertility in females.
Meiotic chromosome associations in homothallic strains of S. cerevisiae were investigated by analysis of meiotic spore colonies and crossing over in +/+/− trisomics. The segregants of these aneuploids produce phenotypically distinguishable tetrasomic spore colonies. The data indicate that trivalent associations occur with a high frequency in trisomics of chromosome XVII and that the frequency of second division segregation is markedly increased over that found in the normal dipoid.
Macronuclei assorting simultaneously for H, Chx, Mpr, and co, and containing only one or two copies of the HD allele produced several combinations of phenotypes at the other loci, instead of only one or two such combinations. It follows that macronuclear subnuclei, if they exist at all, must frequently exchange parts. Models involving somatic recombination, transient subnuclei, or progressive chromosome fragmentation are discussed as possible explanations.
Derivatives of E. coli K12 which had received a number of different drug resistance factors by conjugation from Salmonella strains were found also to have acquired insensitivity to colicins. The insensitivity associated with some R factors was similar in character to immunity conferred by colicinogeny, while that given by others more closely resembled the higher level of resistance due to absence of the colicin receptor. It was, however, not complete. Many of the R factors also restricted the growth of various phages.
The glue proteins are products of a developmentally regulated gene family. These genes are transcriptionally active during the third larval instar and code for the major protein products of salivary glands. The activity of several of the genes can be visualized as intermoult puffs in the polytene salivary gland chromosomes. The amount of one of these proteins, P5, varies widely among wild-type strains. We have used biochemical and genetic methods to investigate the source of this variation. The results of in vitro translation of salivary gland RNA suggest that the variation occurs pretranslationally. Genetic mapping experiments showed that sites on several chromosomes can modulate the amount of P5, but that one site on the third chromosome determines the absence and presence of this protein. We have mapped this glue protein gene, called GP5, to the interval between bx (3–58·8) and sr (3–62·0) which also includes the intermoult puff at 90BC. We discuss the relationship between P5 and the glue protein gene Sgs-5 which is also located at 90BC.
Interest in the selection of mutations affecting L-proline catabolism in Aspergillus nidulans is heightened by the involvement of one of the very few examples of a cluster of functionally related genes in an eukaryote and by an increasing awareness of the biological phenomena in which proline and proline catabolism participate. The sasA-60 (semialdehyde sensitive) mutation in A. nidulans results in toxicity of catabolic precursors of L-glutamic γ-semialdehyde (or its internal Schiff base L-Δ1-pyrroline-5-carboxylate) and succinic semialdehyde, apparently without affecting the catabolic pathways concerned. As sasA-60 is unlinked to the prn gene cluster, specifying the gene products necessary for L-proline catabolism and as L-proline, a precursor of L-glutamic γ-semialdehyde, is highly toxic to sasA-60 strains, this forms the basis of a powerful positive selection technique for obtaining a number of types of prn mutations. Many of these prn mutations can be directly classified according to the gene product(s) affected on the basis of growth phenotype with respect to L-arginine and L-ornithine utilization, proline-dependent resistance to certain toxic amino acid analogues and effect on supplementation of proline auxotrophies. The availability of both a positive selection technique and an extensive nutritional screening system has enabled the identification of fourteen spontaneous deletion mutations, recognized as extending into the prnB gene, specifying the principal L-proline permease, and into at least one other prn gene. These deletion mutations have been partially characterized both genetically and biochemically. In particular their use has greatly facilitated fine-structure mapping of the prn cluster and aided studies of the regulation of prn gene expression.