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T R Wright

Publications and source records attributed to T R Wright.

35 records · Page 2Linked to original sources

The genetics of dopa decarboxylase in Drosophila melanogaster. IV. The genetics and cytology of the 37B10-37D1 region.

Of 204 mutations located in the 8-12 band Df(2L)130 region, 37B9-C1,2;37D1-2, 199 have been assigned to twelve lethal genes and one visible gene (hook). The 13 genes are not evenly distributed. Twelve, (possibly all thirteen) are in the seven band region 37B10-C4 giving a gene-to-band ratio of almost two. Only one gene, 1(2)37Cf, may be in the four band region 37C5-7, and none are localized in band 37D1. In situ hybridization places the dopa decarboxylase structural gene, Ddc, in or very close to band 37C1,2 (Hirsh and Davidson, 1981). The chi methyl dopa hypersensitive gene, 1(2) and, is 0.002 map units distal to Ddc. Df(2L)VA17, 37C1,2; 37F5-38A1 may actually break in the 37C1,2 singlet. It places six genes, hook, 1(2) and, and four lethal genes, in a maximum of five bands, 37B10, 11, 12, 13 and perhaps part of the 37C1,2 singlet and localizes six genes, Ddc plus five lethal genes, in a maximum of three bands; probably part of the 37C1,2 singlet plus bands, C3, and C4. Wild type activity of five of twelve lethal genes is necessary for female fertility. --Band 37C5 puffs at the time of pupariation; Puff Stages 8-10. Twelve of eighteen alleles of 1(2)37Cf have been examined as heterozygotes over CyO and none affect the appearance of a homozygous 37C5 puff. --Of the 204 mutations considered here only one Ddcpl, affects the function of more than one gene. It eliminates Ddc+ and 1(2)37Ca+ function and at 30 degrees C reduces 1(2)37Ce+ function. It is not a deficiency but could be a polar mutant.

Animals↗

The genetics of dopa decarboxylase in Drosophila melanogaster. I. Isolation and characterization of deficiencies that delete the dopa-decarboxylase-dosage-sensitive region and the alpha-methyl-dopa-hypersensitive locus.

A detailed cytogenetic investigation of 16 overlapping deficiencies in the 36C-40A region on the left arm of the second chromosome (2L) in Drosophila melanogaster is reported. These deficiencies permit a localization of both the dopa-decarboxylase-dosage-sensitive region and the alpha-methyl-dopa-hypersensitive locus, l(2) amd, to the same region, 37B10-37C7.

Animals↗

The genetics of dopa decarboxylase in Drosophila melanogaster. II. Isolation and characterization of dopa-decarboxylase-deficient mutants and their relationship to the alpha-methyl-dopa-hypersensitive mutants.

Of 84 lethals isolated over the dopa decarboxylase (DDC) deficiency Df(2L)50, 8 have been identified as DDC-deficient alleles on the basis of their effect on DDC activity when heterozygous over the Cgamma-O balancer chromosome with activities ranging from 28% to 53% of controls. Some of the Ddc-deficient alleles exhibit intracistronic complementation. Most of the complementing pairs of alleles are much reduced in viability, e.g. less than 5% of expected, and express a common syndrome of mutant phenes which can reasonably be inferred to derive from inadequately sclerotinized cuticle. Individuals heterozygous for the noncomplementing allele, Ddcn7, over the 12-band DDC deficiency, Df (2L)130, die at the end of embryogenesis as unhatched larvae with unpigmented mouth parts. The Ddc alleles and the l(2) amd alpha-methyl dopa (alphaMD) hypersensitive alleles are both located within the 11 band region 37B10-C7. The l(2) and locus is immediately to the right of hk(2-53.6). Ddc has been mapped within 0.004 Map Units to the right of l(2) and with a maximum estimated recombination frequency of 0.01%. None of the Ddc/CgammaOstrains are sensitive to the dietary administration of alpha-methyl dopa (alphaMD), and complementation occurs between the Ddc deficient alleles and the l(2) amd alleles both on the basis of viability and DDC activity. No effect on DDC by the amd alleles has been found to date. Even in the complementing heterozygote, amdH1/amdH89, the level of activity, thermostability, and in vitro alphaMD inhibition of DDC remains unaffected. Although no biochemical phene has yet been established for the alphaMD hypersensitive amd alleles, it seems likely that the two groups of mutants are functionally related.

Alleles↗

Cold-sensitive mutants of Drosophila melanogaster defective in ribosome assembly.

Thirteen X-linked, cold-sensitive lethal, female-sterile mutants of Drosophila melanogaster located at eight separate loci were screened for their ability to assemble ribosomes at the restrictive temperature of 17 degrees. Females were labelled with 3H-uridine for either 2 or 20 hours at 17 degrees. A mitochondria-free extract was prepared and analyzed by means of sucrose gradient centrifugation. Four of the mutants, l(1)TW-2cs, l(1)HM16cs, l(1)HM23cs, and l(1)HM20cs, had a lower ratio of cpm in the 40S subunit to cpm in the 60S subunit (40S:60S ratio) than wild type with a 2-hour label. The same was true of a 20-hour label of l(1)TW-2cs, l(1)HM16cs, and l(1)HM23cs, which are allelic, resulted in a 40S:60S ratio higher than wild type. Four other cs mutants were found to have less drastic effects on ribosome assembly. The ribosomal subunits of mutants l(1)HM16cs and l(1)HM20cs sediment at the same rate as their wild-type counterparts. The same is true for the RNA in their ribosomal particles. Sucrose gradient analysis of ribosomes from cold-sensitive lethal, female-sterile mutants appears to be an effective method for finding mutants that affect ribosome assembly.

Animals↗

The developmental genetics of the temperature sensitive lethal allele of the suppressor of forked, 1(1)su(f)ts67g, in Drosophila melanogaster.

A temperature-sensitive lethal allele of suppressor of forked, l(1)su(f)(ts67g) (ts67), has been discovered and characterized as follows: Flies which are hemizygous for ts67 live at 18 degrees and 25 degrees but die at 30 degrees primarily as larvae. The temperature-sensitive period for ts67 homozygotes or hemizygotes begins in second instar and ends at pupation. ts67 is lethal at 30 degrees when heterozygous with suppressor of forked (su(f)), a deficiency for suppressor of forked (su(f)(-)), and a non-conditional lethal allele of suppressor of forked (3DES). It is viable at 30 degrees when heterozygous with the wild-type allele of suppressor of forked. At 25 degrees but not at 18 degrees forked bristles are suppressed in flies of the following genotypes: f(s)ts67/Y, f(s)ts67/f(s)ts67, f(s)ts67/f(s)su(f), f(u)ts67/f(s)3DES, f(u)ts67/f(s)su(f)(-), f(u)ts67/f(s)su(f). There is some suppression of forked bristles at 25 degrees in the heterozygote, f(s)ts67/f(s)+(su(f)). The forked bristle phenotype is not suppressed at either temperature in flies of the genotypes f(u)ts67/Y, f(u)ts67/f(u)ts67/ (f(s) and f(u) indicating suppressible and unsuppressible alleles of forked). The temperature-sensitive period for suppression of forked bristles begins at pupation and extends through the period of bristle synthesis. The deficiency phenotype (bristles reduced in size or absent, wing wrinkled or blistered, eyes rough) typical of flies of the genotype f(s)su(f)/f(s)su(f)(-) at 18 degrees and 25 degrees , is exhibited by flies of the genotypes f(s)ts67/f(s)su(f)(-) at 25 degrees and f(u)ts67/f(s)su(f) at 29 degrees . An allele of lozenge (lz(1)) which can be suppressed by su(f) is suppressed at 25 degrees but not at 18 degrees in lz(1)ts67/Y males. ts67 homozygous females are fertile at 25 degrees but sterile at 30 degrees . The hypothesis is discussed that the su(f) locus codes for a ribosomal protein and that suppression and enhancement are affected by mutations at the locus by mutant ribosome-induced misreading. The possibility is presented that ts67 may be used to determine the translation time in development of any gene.

Alleles↗

A cold-sensitive zygotic lethal causing high frequencies of nondisjunction during meiosis I in Drosophila melanogaster females.

The X-linked, cold-sensitive zygotic lethal, l(1)TW-6(cs), both in homozygous and heterozygous females, induces nondisjunction of all four chromosomes at Meiosis I at both 25 degrees and 17 degrees . Nondisjunction frequencies approaching 0.5 for the X and fourth chromosomes have been observed at 16 degrees -18 degrees . The disjunction of the X chromosomes in males is not affected. The mutant causes mitotic irregularities in zygotes at both 25 degrees and 17 degrees . Mortality of all zygotes produced by the crosses 6(cs)/6(cs)x6(cs)/B(s)Y and FM7/6(cs)x6(cs)/B(s)Y is respectively 86% and 67-74% at 25 degrees and 99.8-99.9% and 94% at 17 degrees . The mortality of 6(cs) hemizygotes derived from females carrying no doses of 6(cs) (C(1)DX,y f/yx6(cs)/B(s)Y) is 45-55% at 25 degrees and 98% at 17 degrees . The length of the temperature-sensitive period for 6(cs) homo- and hemizygotes is affected by the maternal dosage of 6(cs); the shortest TSP is for zero and the longest is for two maternal doses. Mortality takes place primarily during embryogenesis with some larval and little pupal mortality. Analysis of sectioned embryos indicates that the large array of different patterns of damage observed could have arisen from abnormal cleavage divisions and the incomplete population of the blastoderm with nuclei.

Animals↗

The Wilhelmine E. Key 1992 Invitational lecture. Phenotypic analysis of the Dopa decarboxylase gene cluster mutants in Drosophila melanogaster.

Mutations in a majority of the 18 loci of the Dopa decarboxylase (Ddc) gene cluster effect similar morphological defects of the cuticle and/or catecholamine-related abnormalities. Mutations in 14 loci affect cuticle formation, cuticle sclerotization, or cuticle melanization, with mutations in 11 of these same loci (including Ddc and amd) producing melanotic psueudotumors, symptomatic, perhaps, of abnormal catecholamine metabolism. Mutations in seven of the genes perturb catecholamine pool levels during prepupal and pupal development, all of which also form melanotic pseudotumors, suggesting several of these genes may encode proteins involved in catecholamine metabolism. Thus, the Ddc gene cluster represents in higher eukaryotes an unusual example of a large cluster of functionally related genes involved in a common physiological process.

Animals↗