scholarly journals Three neighboring genes interact with the Broad-Complex and the Stubble-stubbloid locus to affect imaginal disc morphogenesis in Drosophila.

Genetics ◽  
1991 ◽  
Vol 127 (4) ◽  
pp. 747-759 ◽  
Author(s):  
P J Gotwals ◽  
J W Fristrom

Abstract The Broad-Complex (BR-C) is a complex regulatory locus at 2B-5 on the X chromosome of Drosophila melanogaster. The wild-type BR-C products are apparent transcription factors necessary for imaginal disc morphogenesis. Alleles of the Stubble-stubbloid (Sb-sbd) locus at 89B9-10 act as dominant enhancers of broad alleles of the BR-C. Sb-sbd wild-type products are necessary for appendage elongation. We report, here, on three new loci implicated in imaginal disc morphogenesis based on their genetic interactions with both BR-C and/or Sb-sbd mutants. Enhancer of broad (E(br)) was identified as a dominant enhancer of the br1 allele of the BR-C and is a recessive lethal. Mapping of E(br) has led to the identification of two loci, blistered and l(2)B485, mutants of which interact with E(br) and the Sb-sbd locus. Blistered, but not l(2)B485, interacts strongly with the BR-C. Alleles of the blistered locus are viable and disrupt proper wing disc morphogenesis independent of genetic interactions. All three loci map within the 0.6-map unit interval between the genetic markers speck and Irregular facets and to the cytological region 60C5-6; 60E9-10 at the tip of chromosome 2R. Genetic evidence is consistent with the view that the BR-C regulates blistered.

Genetics ◽  
1988 ◽  
Vol 120 (2) ◽  
pp. 453-464
Author(s):  
A H Beaton ◽  
I Kiss ◽  
D Fristrom ◽  
J W Fristrom

Abstract The 2B5 region on the X chromosome of Drosophila melanogaster forms an early ecdysone puff at the end of the third instar. The region is coextensive with a complex genetic locus, the Broad-Complex (BR-C). The BR-C is a regulatory gene that contains two major functional domains, the br domain and the l(1)2Bc domain. BR-C mutants prevent metamorphosis, including morphogenesis of imaginal discs; br mutants prevent elongation and eversion of appendages and l(1)2Bc mutants prevent fusion of the discs. The Stubble-stubbloid (Sb-sbd) locus at 89B9-10 is best known for the effects of its mutants on bristle structure. Mutants of the BR-C and the Sb-sbd locus interact to produce severe malformation of appendages. Viable heteroallelic and homoallelic combinations of Sb-sbd mutants, including loss-of-function mutants, affect the elongation of imaginal disc appendages. Thus, the Sb-sbd+ product is essential for normal appendage elongation. Sb-sbd mutants, however, do not affect eversion or fusion of discs. Correspondingly, only BR-C mutants deficient in br function interact with Sb-sbd mutants. The interaction occurs in deficiency heterozygotes using single, wild-type doses of the BR-C, of the Sb-sbd locus, or of both loci. These last results are formally consistent with the possibility that the BR-C acts as a positive regulator of the Sb-sbd locus. The data do not exclude other possible nonregulatory interactions between the two loci, e.g., interactions between the products of both genes.


1977 ◽  
Vol 32 (1-2) ◽  
pp. 125-132 ◽  
Author(s):  
Karl Georg Götz ◽  
Simon Götz

Abstract Attempts to substantiate irreversible actions of a variety of magnetic fields on the fruitfly, Drosophila melanogaster, have been successful and unsuccessful in about equal numbers. The most conspicuous mutagenic effects apparently induced by pulsed H F-fields failed to appear under continuous electromagnetic irradiation. This seems to correlate the observed damage with the VLF-components of the pulsed fields. The present investigation is motivated by the occurrence of these components both in the atmosphere and in the vicinity of electrical appliances. A strain of normally viable wild type males and subnormally viable Attached-X γ ω females was used in which the yield, and the sex ratio, of the progeny indicate, respectively, the extent of developmental damage and of sex-linked recessive lethal mutation induced by the exposure to detrimental conditions. Evaluation of 73,800 flies from subsequent generations of a control group and two test groups raised in steady, or rotating, homogeneous 9.6 kHz magnetic fields of about 2.5 G did not reveal any development of hereditare load in the test groups.


2010 ◽  
Vol 8 (3) ◽  
pp. 67-80 ◽  
Author(s):  
Aleksey A Moskalev ◽  
Olga A Malysheva

It was investigated the role of stress-response genes (dFOXO, dSir2, Hsp70) in regulation of life span of Drosophila in response to light regime alteration. It was revealed the FOXO-dependant mechanism of lifespan increasing at darkness conditions. The distance of lifespan of FOXO homozygous mutants at different light conditions were absent 3 times from 4 times. It was shown, that homozygotes with deletion of dSir2 have more significant difference between lifespan at standard light and darkness conditions with comparing to wild type and heterozygous strain. The same tendency was also detected the in the strains with Hsp70 deletions. It was produced the evidences of two mechanisms of light regime influence on lifespan: metabolism intensification at light conditions and neuroendocrine-determinated lifespan increasing at darkness conditions.


1952 ◽  
Vol 30 (6) ◽  
pp. 375-377 ◽  
Author(s):  
D. P. Pielou

As experiments are in progress on selective breeding for insecticide tolerance in insect parasites and as various physiologically potent chemicals have been shown to cause mutation in Drosophila melanogaster Meig., tests were made to determine whether p-p′-DDT and γ-hexachlorocyclohexane had any mutagenic action. Wild type males of D. melanogaster that had been exposed to the former insecticide in their larval feeding medium, or, as adults, to the vapor of the latter insecticide, were tested. The Muller-5 method of detecting recessive lethal mutations in the X chromosome was used. No evidence of mutagenic action was found in either insecticidal isomer.


Genetics ◽  
1995 ◽  
Vol 141 (3) ◽  
pp. 1037-1042 ◽  
Author(s):  
D R Dorer ◽  
D H Ezekiel ◽  
A C Christensen

Abstract In the genome of Drosophila melanogaster there is a single locus, Triplo-lethal (Tpl), that causes lethality when present in either one or three copies in an otherwise diploid animal. Previous attempts to mutagenize Tpl produced alleles that were viable over a chromosome bearing a duplication of Tpl, but were not lethal in combination with a wild-type chromosome, as deficiencies for Tpl are. These mutations were interpreted as hypomorphic alleles of Tpl. In this work, we show that these alleles are not mutations at Tpl; rather, they are dominant mutations in a tightly linked, but cytologically distant, locus that we have named Suppressor-of-Tpl (Sul(Tpl)). Su(Tpl) mutations suppress the lethality associated with three copies of the Triplo-lethal locus and are recessive lethal. We have mapped Su(Tpl) to the approximate map position 3-46.5, within the cytological region 76B-76D.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Lijuan Du ◽  
Alex Sohr ◽  
Ge Yan ◽  
Sougata Roy

Gradients of signaling proteins are essential for inducing tissue morphogenesis. However, mechanisms of gradient formation remain controversial. Here we characterized the distribution of fluorescently-tagged signaling proteins, FGF and FGFR, expressed at physiological levels from the genomic knock-in alleles in Drosophila. FGF produced in the larval wing imaginal-disc moves to the air-sac-primordium (ASP) through FGFR-containing cytonemes that extend from the ASP to contact the wing-disc source. The number of FGF-receiving cytonemes extended by ASP cells decreases gradually with increasing distance from the source, generating a recipient-specific FGF gradient. Acting as a morphogen in the ASP, FGF activates concentration-dependent gene expression, inducing pointed-P1 at higher and cut at lower levels. The transcription-factors Pointed-P1 and Cut antagonize each other and differentially regulate formation of FGFR-containing cytonemes, creating regions with higher-to-lower numbers of FGF-receiving cytonemes. These results reveal a robust mechanism where morphogens self-generate precise tissue-specific gradient contours through feedback regulation of cytoneme-mediated dispersion.


Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1833-1843 ◽  
Author(s):  
Ajay Srivastava ◽  
Andrew J Simmonds ◽  
Ankush Garg ◽  
Leif Fossheim ◽  
Shelagh D Campbell ◽  
...  

Abstract The Drosophila melanogaster scalloped (sd) gene is a homolog of the human TEF-1 gene and is a member of the TEA/ATTS domain-containing family of transcription factors. In Drosophila, sd is involved in wing development as well as neural development. Herein, data are presented from a molecular analysis of five recessive lethal sd alleles. Only one of these alleles complements a viable allele associated with an sd mutant wing phenotype, suggesting that functions important for wing development are compromised by the noncomplementing alleles. Two of the wing noncomplementing alleles have mutations that help to define a VG-binding domain for the SD protein in vivo, and another noncomplementing allele has a lesion within the TEA DNA-binding domain. The VG-binding domain overlaps with a domain important for viability of the fly, since two of the sd lethal lesions are located there. The fifth lethal affects a yet undefined motif lying just outside the VG-binding domain in the C-terminal direction that affects both wing phenotype and viability. This is the first example linking mutations affecting specific amino acids in the SD protein with phenotypic consequences for the organism.


1975 ◽  
Vol 17 (3) ◽  
pp. 423-432 ◽  
Author(s):  
David T. Kuhn ◽  
Suzanne F. Dorgan

Homoeotic effects (one organ replaced by an organ from a different part of the body) were investigated in the tumorous-head phenotype in Drosophila melanogaster. The tumorous-head mutant is the only known maternally effected homoeotic mutant (Postlethwait and Schneiderman, 1973). As reported by Postlethwait et al. (1972) transformations from eye to abdominal like structures, eye to antennal like structures, eye to palpus like structures, rostralhaut to genital like structures, rostralhaut to clasper teeth, and rostralhaut to antennal like structures were observed. Transformations currently observed but not by Postlethwait et al. (1972) are: eye to genital structures (resembling anal plates in both sexes or lateral plates in males); antenna to genital like structures; rostralhaut to abdominal like structures; and proboscis to leg like structures. Since a tumorous-head strain selected for high penetrance and expressivity was used for this study, differences between the two studies are ascribed to strain selection. Effect of a third chromosome gene which acts to enhance the tumorous-head maternal effect was also investigated. A highly significant increase in expressivity was found especially in females. Of 4,730 female flies examined possessing the enhancer gene, high penetrance and high expressivity, only the eye-antennal imaginal disc and possibly the libial disc showed destabilization. We observed no destabilization of the wing disc by the tumorous-head genes as predicted by Kauffman (1973).


Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 657-670
Author(s):  
Michael A Buratovich ◽  
Peter J Bryant

Recessive lethal mutations of the lethal(2)giant discs (l(2)gd) and lethal(2)fat (l(2)ft) loci of Drosophila melanogaster cause imaginal disc hyperplasia during a prolonged larval stage. Imaginal discs from l(2)ft l(2)gd or G l(2)gd double homozygotes show more extensive overgrowth than in either single homozygote, and double homozygous l(2)ft l(2)gd mitotic clones in adult flies show much more overgrowth than is seen in clones homozygous for either l(2)gd or l(2)ft alone. dachsous (ds) also acts as an enhancer of l(2)gd, producing dramatically overgrown discs and causing failure to pupariate in double homozygotes. The comb gap (cg) mutation, which also interacts with ds, greatly enhances the tendency of imaginal discs from l(2)gd larvae to duplicate as they overgrow. If l(2)gd homozygotes are made heterozygous for l(2)ft, then several discs duplicate, indicating that l(2)ft acts as a dominant enhancer of l(2)gd. l(2)ft also acts as a dominant enhancer of l(2)gd, and conversely l(2)gd acts as a dominant modifier of l(2)ft. The enhancement of overgrowth caused by various mutant combinations is accompanied by changes in expression of Decapentaplegic and Wingless. These results show that tumor suppressor genes act in combination to control cell proliferation, and that tissue hyperplasia can be associated with ectopic expression of genes involved in pattern formation.


Genetics ◽  
1978 ◽  
Vol 89 (2) ◽  
pp. 355-370 ◽  
Author(s):  
Allen Shearn ◽  
Grafton Hersperger ◽  
Evelyn Hersperger ◽  
Ellen Steward Pentz ◽  
Paul Denker

ABSTRACT The phenotypes of five different lethal mutants of Drosophila melanogaster that have small imaginal discs were analyzed in detail. From these results, we inferred whether or not the observed imaginal disc phenotype resulted exclusively from a primary imaginal disc defect in each mutant. To examine the validity of these inferences, we employed a multiple-allele method. Lethal alleles of the five third-chromosome mutations were identified by screening EMS-treated chromosomes for those which fail to complement with a chromosome containing all five reference mutations. Twenty-four mutants were isolated from 13,197 treated chromosomes. Each of the 24 was then tested for complementation with each of the five reference mutants. There was no significant difference in the mutation frequencies at these five loci. The stage of lethality and the imaginal disc morphology of each mutant allele were compared to those of its reference allele in order to examine the range of defects to be found among lethal alleles of each locus. In addition, hybrids of the alleles were examined for intracistronic complementation. For two of the five loci, we detected no significant phenotypic variation among lethal alleles. We infer that each of the mutant alleles at these two loci cause expression of the null activity phenotype. However, for the three other loci, we did detect significant phenotypic variation among lethal alleles. In fact, one of the mutant alleles at each of these three loci causes no detectable imaginal disc defect. This demonstrates that attempting to assess the developmental role of a gene by studying a single mutant allele may lead to erroneous conclusions. As a byproduct of the mutagenesis procedure, we have isolated two dominant, cold-sensitive mutants.


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