scholarly journals Physiological genetics of melanotic tumours in Drosophila melanogaster: VIII. The role of choline in the expression of the tumour gene tu bw and of its suppressor, su-tu

1974 ◽  
Vol 24 (2) ◽  
pp. 215-227 ◽  
Author(s):  
John C. Sparrow ◽  
James H. Sang
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Product ◽  
Biochemical Pathway ◽  
Phospholipid Synthesis ◽  
Axenic Medium ◽  
Metabolic Functions ◽  
Melanotic Tumour ◽  
Strain Responses

SUMMARYThe melanotic tumour gene tu bw of Drosophila melanogaster has a specific suppressor su-tu. The genotypes tu bw; +su-tu and tu bw; su-tu show opposite responses, as measured by tumour penetrance, to increasing choline levels in the defined axenic medium. The three major metabolic functions of choline have been examined using additions to the axenic medium to determine which biochemical pathway(s) are different in the two genotypes. It is concluded that the opposite strain responses are due to changes in the pattern of phospholipid synthesis, and that the gene product of the su-tu gene probably functions in this area of metabolism.

Control of expression of the homeotic labial (lab) locus of Drosophila melanogaster: evidence for both positive and negative autogenous regulation

Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1267-1280 ◽  
Author(s):  
S. Chouinard ◽  
T.C. Kaufman
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Product ◽  
Expression Pattern ◽  
Embryonic Lethality ◽  
Sensory Cells ◽  
Homeotic Genes ◽  
Aberrant Expression ◽  
Adult Head ◽  
Antennal Disc

The homeotic gene labial (lab) is required for proper development of the embryonic and adult head in Drosophila melanogaster. The lab gene product accumulates in a complex pattern in both embryonic and imaginal tissue. During embryogenesis, lab is expressed in the endodermally derived cells of the midgut, in ectodermally derived cells of the procephalon and dorsal ridge, and in a small subset of progenitor sensory cells. Imaginal expression is restricted to a narrow region of the peripodial membrane of the eye-antennal disc. As part of our continuing effort to understand the role of lab in development, we have begun a dissection of the regulatory elements of the lab transcription unit and used germ line transformation experiments to determine which aspects of the observed expression pattern are essential for proper head development and viability. Transgenic embryos harboring an abridged lab gene are able to overcome the embryonic lethality associated with the loss of lab function and survive to adulthood. Interestingly, in these transgenic lines the lab protein accumulates only in a subset of those embryonic cells that normally express the gene, namely the procephalon and the anterior midgut. We also find that, once initiated, lab expression is maintained by positive autoregulation. Although lab minigene activity is sufficient to rescue the embryonic lethality of lab mutations, the transgenes fail to rescue defects in the adult head capsule. However, the defects observed in this study encompass a broader domain than those seen using somatic recombination to generate lab- clonal tissue. The failed rescue and observed cuticular defects are, at least in part, explained by the observation that the transgenes, rather than failing to be expressed, are associated with ectopic accumulation of lab protein in the peripodial membrane of the antennal disc. Moreover, this aberrant expression pattern is correlated with the abnormal expression of two other homeotic genes, Deformed (Dfd) and Sex combs reduced (Scr) in the eye-antennal disc. These results are only observed when the transgene is resident in a lab- genotype and ectopic expression of lab and misregulation of Dfd and Scr are not seen in a lab+ background. This result suggests that the wild-type lab gene product is necessary for the normal regulation of the locus in the imaginal discs, but unlike the case in the embryo, the event is negative. We discuss the biological implications of these results in relation to the role of lab in development.

scholarly journals MULTIPLE ALLELE APPROACH TO THE STUDY OF GENES IN DROSOPHILA MELANOGASTER THAT ARE INVOLVED IN IMAGINAL DISC DEVELOPMENT

Genetics ◽  
1978 ◽  
Vol 89 (2) ◽  
pp. 355-370 ◽  
Author(s):  
Allen Shearn ◽  
Grafton Hersperger ◽  
Evelyn Hersperger ◽  
Ellen Steward Pentz ◽  
Paul Denker
Keyword(s):  
Drosophila Melanogaster ◽  
Phenotypic Variation ◽  
Mutant Allele ◽  
Imaginal Disc ◽  
Reference Allele ◽  
Multiple Allele ◽  
Significant Difference ◽  
Chromosome Mutations ◽  
Cold Sensitive

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.

scholarly journals Dual roles for the Drosophila PI 4-kinase Four wheel drive in localizing Rab11 during cytokinesis

2009 ◽  
Vol 187 (6) ◽  
pp. 847-858 ◽  
Author(s):  
Gordon Polevoy ◽  
Ho-Chun Wei ◽  
Raymond Wong ◽  
Zsofia Szentpetery ◽  
Yeun Ju Kim ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Critical Role ◽  
Successful Completion ◽  
Dual Roles ◽  
Recycling Endosome ◽  
Golgi Membranes ◽  
Wheel Drive ◽  
Dividing Cells ◽  
Four Wheel Drive

Successful completion of cytokinesis relies on addition of new membrane, and requires the recycling endosome regulator Rab11, which localizes to the midzone. Despite the critical role of Rab11 in this process, little is known about the formation and composition of Rab11-containing organelles. Here, we identify the phosphatidylinositol (PI) 4-kinase III β Four wheel drive (Fwd) as a key regulator of Rab11 during cytokinesis in Drosophila melanogaster spermatocytes. We show Fwd is required for synthesis of PI 4-phosphate (PI4P) on Golgi membranes and for formation of PI4P-containing secretory organelles that localize to the midzone. Fwd binds and colocalizes with Rab11 on Golgi membranes, and is required for localization of Rab11 in dividing cells. A kinase-dead version of Fwd also binds Rab11 and partially restores cytokinesis to fwd mutant flies. Moreover, activated Rab11 partially suppresses loss of fwd. Our data suggest Fwd plays catalytic and noncatalytic roles in regulating Rab11 during cytokinesis.

scholarly journals Role of the Deubiquitylating Enzyme DmUsp5 in Coupling Ubiquitin Equilibrium to Development and Apoptosis in Drosophila melanogaster

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120875 ◽  
Author(s):  
Levente Kovács ◽  
Olga Nagy ◽  
Margit Pál ◽  
Andor Udvardy ◽  
Octavian Popescu ◽  
...  
Keyword(s):  
Drosophila Melanogaster

The P-element-induced silencing effect of KP transposons is dose dependent in Drosophila melanogaster

Genome ◽  
2011 ◽  
Vol 54 (9) ◽  
pp. 752-762 ◽  
Author(s):  
Alireza Sameny ◽  
John Locke
Keyword(s):  
Drosophila Melanogaster ◽  
Critical Role ◽  
Mutagenic Effect ◽  
P Element ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
P Elements ◽  
Single Well ◽  
Dose Dependent

Transposable elements are found in the genomes of all eukaryotes and play a critical role in altering gene expression and genome organization. In Drosophila melanogaster, transposable P elements are responsible for the phenomenon of hybrid dysgenesis. KP elements, a deletion-derivative of the complete P element, can suppress this mutagenic effect. KP elements can also silence the expression of certain other P-element-mediated transgenes in a process called P-element-dependent silencing (PDS), which is thought to involve the recruitment of heterochromatin proteins. To explore the mechanism of this silencing, we have mobilized KP elements to create a series of strains that contain single, well-defined KP insertions that show PDS. To understand the quantitative role of KP elements in PDS, these single inserts were combined in a series of crosses to obtain genotypes with zero, one, or two KP elements, from which we could examine the effect of KP gene dose. The extent of PDS in these genotypes was shown to be dose dependent in a logarithmic rather than linear fashion. A logarithmic dose dependency is consistent with the KP products interacting with heterochromatic proteins in a concentration-dependent manner such that two molecules are needed to induce gene silencing.

The role of Su(Hw) protein in transcription regulation in Drosophila melanogaster

2015 ◽  
Vol 51 (11) ◽  
pp. 1060-1068
Author(s):  
P. V. Elizar’ev ◽  
D. A. Chetverina ◽  
A. K. Golovnin ◽  
P. G. Georgiev ◽  
M. M. Erokhin
Keyword(s):  
Drosophila Melanogaster ◽  
Transcription Regulation

Multigene Family of Ribosomal DNA in Drosophila melanogaster Reveals Contrasting Patterns of Homogenization for IGS and ITS Spacer Regions: A Possible Mechanism to Resolve This Paradox

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 243-256 ◽  
Author(s):  
Carlos Polanco ◽  
Ana I González ◽  
Álvaro de la Fuente ◽  
Gabriel A Dover
Keyword(s):  
Drosophila Melanogaster ◽  
Concerted Evolution ◽  
Multigene Family ◽  
Natural Populations ◽  
Intergenic Spacer ◽  
Meiotic Pairing ◽  
Y Chromosomes ◽  
Mutation Distribution ◽  
Chromosome Exchanges

Abstract The multigene family of rDNA in Drosophila reveals high levels of within-species homogeneity and between-species diversity. This pattern of mutation distribution is known as concerted evolution and is considered to be due to a variety of genomic mechanisms of turnover (e.g., unequal crossing over and gene conversion) that underpin the process of molecular drive. The dynamics of spread of mutant repeats through a gene family, and ultimately through a sexual population, depends on the differences in rates of turnover within and between chromosomes. Our extensive molecular analysis of the intergenic spacer (IGS) and internal transcribed spacer (ITS) spacer regions within repetitive rDNA units, drawn from the same individuals in 10 natural populations of Drosophila melanogaster collected along a latitudinal cline on the east coast of Australia, indicates a relatively fast rate of X-Y and X-X interchromosomal exchanges of IGS length variants in agreement with a multilineage model of homogenization. In contrast, an X chromosome-restricted 24-bp deletion in the ITS spacers is indicative of the absence of X-Y chromosome exchanges for this region that is part of the same repetitive rDNA units. Hence, a single lineage model of homogenization, coupled to drift and/or selection, seems to be responsible for ITS concerted evolution. A single-stranded exchange mechanism is proposed to resolve this paradox, based on the role of the IGS region in meiotic pairing between X and Y chromosomes in D. melanogaster.

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