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At least 721 records · Page 40Linked to original sources
PubMed1994

Genetic characterization of Drosophila RBP-J kappa (suppressor of hairless) as a neurogenic gene in adult PNS development.

Drosophila RBP-J kappa is a novel sequence-specific DNA binding protein encompassing the integrase motif which is highly conserved in various organisms. Its gene has been shown to be identical to Suppressor of Hairless which regulates adult peripheral nervous system (PNS) development. To elucidate the precise function of the RBP-J kappa protein in adult PNS development, we analyzed transgenic files that misexpress the RBP-J kappa protein. Such studies have shown that RBP-J kappa regulates PNS cell fate in at least two steps: commitment to sensory mother cell by lateral inhibition and terminal differentiation into the socket and shaft cells. Taken together with analysis of phenotypes of Suppressor of Hairless mutants, RBP-J kappa shows the synergistic activity with neurogenic genes.

Animals↗
PubMed1995

P element-induced mutations in Drosophila melanogaster showing high interspecific crossability between D. melanogaster females and D. simulans males.

Homozygous stocks for the second or the third chromosome of Drosophila melanogaster with a single insertional plwB element were screened for high crossability with D. simulans. Reciprocal crosses between each of these stocks and D. simulans were made, and the insemination rate at two or three days was examined. From two cycles of screening of the original 575 stocks, one stock (# 687) which showed high insemination rate was selected and was backcrossed to a w strain to substitute the background. We obtained a stock which showed 10% insemination rate with D. simulans males (control was 0%). No stocks exhibiting a high crossability with D. simulans females were acquired. Revertant strains, from which the P element had been lost, were obtained from the backcrossed # 687 stock. The insemination rates of 13 revertants to D. simulans males ranged from 1% to 33%. Seven of these 13 were not significantly different from the control line but were significantly different from the backcrossed # 687 stock. It was concluded that the mutation showing high crossability with D. simulans males was caused by the P element transposition.

Animals↗
PubMed1995

Molecular and genetic dissection of a reproductive isolation gene, zygotic hybrid rescue, of Drosophila melanogaster.

Hybrids from the cross between males of Drosophila melanogaster and females of its sibling species (D. simulans, D. mauritiana, or D. sechellia) are embryonic lethal when they carry the wild type allele of zygotic hybrid rescue (zhr) from D. melanogaster. The zhr gene has been mapped in the proximal region of the X heterochromatin slightly distal to the proximal breakpoint of In(1)sc8, the region rich in 1.688 g/cm3 satellite DNA. Since this satellite DNA does not exist in the sibling species, the satellite DNA was considered to be involved in the hybrid lethality. We examined the hypothesis molecular cytogenetically. The results are (1) three Df(1)zhr chromosomes carried this satellite DNA, and (2) hybrids were viable even if the amount of the satellite DNA in hybrids was increased by adding minichromosomes Dp(1;f)1205 and Dp(1;f)1187 into the genome. These results do not support the above hypothesis.

Alleles↗
PubMed1995

Suppressor of hairless, the Drosophila homologue of RBP-J kappa, transactivates the neurogenic gene E(spl)m8.

Suppressor of Hairless[Su(H)], the Drosophila homologue of RBP-J kappa is a novel type of sequence-specific DNA binding protein without known motifs, and highly conserved in various organisms. Su(H) regulates peripheral nervous system (PNS) development. Recently Su(H) was suggested to participate in the Notch-mediated signal transduction pathway. We show here that the Su(H) protein binds to TGTGGGAA sequence located 616 base-pairs upstream of the transcription initiation site of the Enhancer of split [E(spl)]m8 gene which is mapped to the terminus of the genetic cascade of the neurogenic genes. Su(H) transactivates the E(spl)m8 promoter not only in cultured Drosophila cells but also in vivo. The present study bridges the biochemical gap between Notch and E(spl) in the neurogenic gene cascade including Delta, Notch, deltex, Su(H), Hairless and E(spl).

Alleles↗
PubMed1998

Mitochondrial localization and temporal expression of the Drosophila melanogaster DnaJ homologous tumor suppressor Tid50.

The Drosophila melanogaster tumor suppressor gene lethal(2)tumorous imaginal discs (tid) was identified as a homolog of all dnaJ-like genes known to date which have been well preserved in evolution. Homozygous D. melanogaster l(2)tid mutants l(2)tid1, l(2)tid2 and l(2)tid3 are characterized by neoplastic transformation of the adult integumental primordia, the imaginal discs, and the death at the time of puparium formation. The first part of this study is concerned with the identification and subcellular localization of the l(2)tid-encoded protein, Tid50. The second part examines its tissue specific expression during wild-type development and in tumorous imaginal discs. To specify the function(s) of the Tid50 protein polyclonal rabbit antibodies directed against various domains of it were generated and used for staining of Western blots and whole-mounts and paraffin sections of various tissues isolated from wild-type and mutant tumor-developing animals. To identify the mutational events leading in homozygous l(2)tid mutants to abnormal expression level of l(2)tid-encoded RNA and protein, the mutant gene was isolated from homozygous l(2)tid1 and l(2)tid2 animals and sequenced.

Animals↗
PubMed2005

Expression of mdr49 and mdr65 multidrug resistance genes in larval tissues of Drosophila melanogaster under normal and stress conditions.

In situ expression of 2 multidrug resistance genes, mdr49 and mdr65, of Drosophila melanogaster was examined in wild-type third instar larval tissues under physiological conditions and after heat shock or colchicine feeding. Expression of these 2 genes was also examined in tumorous tissues of lethal (2) giant larvae I(2)gl4 mutant larvae. These 2 mdr genes show similar constitutive expression in different larval tissues under physiological conditions. However, they are induced differentially by endogenous (tumorous growth) and exogenous stresses (colchcine feeding or heat shock): whereas heat shock and colchicine feeding induce mdr49, tumorous condition is accompanied by enhanced expression of mdr49 and mdr65 genes.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2004

Dynamics of decapentaplegic expression during regeneration of the Drosophila melanogaster wing imaginal disc.

Regeneration of an imaginal disc involves highly ordered proliferation and pattern regulation of the newly formed tissue. Although the general principles of imaginal disc regeneration have been extensively studied, knowledge of the underlying molecular mechanisms is far from complete. Results from other model organisms suggest that regeneration is the result of local recapitulation of the normal patterning genes. To analyze the dynamics of one major Drosophila patterning gene, decapentaplegic (dpp), in wing imaginal disc regeneration, a vital GFP reporter together with iontophoretic cell labeling were used. Our observations reveal that the restoration of compartment-border-specific dpp expression is a common event in imaginal disc regeneration. However, we did not find evidence of an upregulation of dpp expression during the regeneration process.

Animals↗
PubMed2004

Trans-splicing of the mod(mdg4) complex locus is conserved between the distantly related species Drosophila melanogaster and D. virilis.

The modifier of mdg4, mod(mdg4), locus in Drosophila melanogaster represents a new type of complex gene in which functional diversity is resolved by mRNA trans-splicing. A protein family of >30 transcriptional regulators, which are supposed to be involved in higher-order chromatin structure, is encoded by both DNA strands of this locus. Mutations in mod(mdg4) have been identified independently in a number of genetic screens involving position-effect variegation, modulation of chromatin insulators, apoptosis, pathfinding of nerve cells, and chromosome pairing, indicating pleiotropic effects. The unusual gene structure and mRNA trans-splicing are evolutionary conserved in the distantly related species Drosophila virilis. Chimeric mod(mdg4) transcripts encoded from nonhomologous chromosomes containing the splice donor from D. virilis and the acceptor from D. melanogaster are produced in transgenic flies. We demonstrate that a significant amount of protein can be produced from these chimeric mRNAs. The evolutionary and functional conservation of mod(mdg4) and mRNA trans-splicing in both Drosophila species is furthermore demonstrated by the ability of D. virilis mod(mdg4) transgenes to rescue recessive lethality of mod(mdg4) mutant alleles in D. melanogaster.

Alleles↗
PubMed2006

Misregulation of sex-lethal and disruption of male-specific lethal complex localization in Drosophila species hybrids.

A major model system for the study of evolutionary divergence between closely related species has been the unisexual lethality resulting from reciprocal crosses of Drosophila melanogaster and D. simulans. Sex-lethal (Sxl), a critical gene for sex determination, is misregulated in these hybrids. In hybrid males from D. melanogaster mothers, there is an abnormal expression of Sxl and a failure of localization of the male-specific lethal (MSL) complex to the X chromosome, which causes changes in gene expression. Introduction of a Sxl mutation into this hybrid genotype will allow expression of the MSL complex but there is no sequestration to the X chromosome. Lethal hybrid rescue (Lhr), which allows hybrid males from this cross to survive, corrects the SXL and MSL defects. The reciprocal cross of D. simulans mothers by D. melanogaster males exhibits underexpression of Sxl in embryos.

Animals↗
PubMed2006

Genes affecting cell competition in Drosophila.

Cell competition is a homeostatic mechanism that regulates the size attained by growing tissues. We performed an unbiased genetic screen for mutations that permit the survival of cells being competed due to haplo-insufficiency for RpL36. Mutations that protect RpL36 heterozygous clones include the tumor suppressors expanded, hippo, salvador, mats, and warts, which are members of the Warts pathway, the tumor suppressor fat, and a novel tumor-suppressor mutation. Other hyperplastic or neoplastic mutations did not rescue RpL36 heterozygous clones. Most mutations that rescue cell competition elevated Dpp-signaling activity, and the Dsmurf mutation that elevates Dpp signaling was also hyperplastic and rescued. Two nonlethal, nonhyperplastic mutations prevent the apoptosis of Minute heterozygous cells and suggest an apoptosis pathway for cell competition . In addition to rescuing RpL36 heterozygous cells, mutations in Warts pathway genes were supercompetitors that could eliminate wild-type cells nearby. The findings show that differences in Warts pathway activity can lead to competition and implicate the Warts pathway, certain other tumor suppressors, and novel cell death components in cell competition, in addition to the Dpp pathway implicated by previous studies. We suggest that cell competition might occur during tumor development in mammals.

Animals↗
PubMed2006

In vivo construction of transgenes in Drosophila.

Transgenic flies are generated by transposon-mediated transformation. A drawback of this approach is the size limit of transposable elements. Here, we propose a novel method that allows the extension of transgenes in vivo. This method is based on an incomplete transgene that has been constructed in vitro and integrated into the Drosophila genome by conventional transgenesis. The incomplete transgene contains two short stretches of DNA homologous to the 5'- and 3'-ends of a larger DNA segment of interest. Between the short stretches of homology an I-SceI recognition site is located. Once activated, I-SceI endonuclease introduces a DNA double-strand break, which triggers ectopic recombination between the stretches of homology and the endogenous locus. Through gap repair, the transgene obtains the complete region of interest in vivo. Our results show that this method is effective for copying up to 28 kb of genomic DNA into the transgene, thereby eliminating the technical difficulties associated with the in vitro construction of large transgenes and extending the size limits of current transgenesis protocols. In general, this method may be a useful technique for genetic engineering of eukaryotic model organisms.

Animals↗
PubMed2004

Genetic dissection of itpr gene function reveals a vital requirement in aminergic cells of Drosophila larvae.

Signaling by the second messenger inositol 1,4,5-trisphosphate is thought to affect several developmental and physiological processes. Mutants in the inositol 1,4,5-trisphosphate receptor (itpr) gene of Drosophila exhibit delays in molting while stronger alleles are also larval lethal. In a freshly generated set of EMS alleles for the itpr locus we have sequenced and identified single point mutations in seven mutant chromosomes. The predicted allelic strength of these mutants matches the observed levels of lethality. They range from weak hypomorphs to complete nulls. Interestingly, lethality in three heteroallelic combinations has a component of cold sensitivity. The temporal focus of cold sensitivity lies in the larval stages, predominantly at second instar. Coupled with our earlier observation that an itpr homozygous null allele dies at the second instar stage, it appears that there is a critical period for itpr gene function in second instar larvae. Here we show that the focus of this critical function lies in aminergic cells by rescue with UAS-itpr and DdCGAL4. However, this function does not require synaptic activity, suggesting that InsP(3)-mediated Ca(2+) release regulates the neurohormonal action of serotonin.

Alleles↗
PubMed2004

The Drosophila GAGA factor is required for dosage compensation in males and for the formation of the male-specific-lethal complex chromatin entry site at 12DE.

Drosophila melanogaster males have one X chromosome, while females have two. To compensate for the resulting disparity in X-linked gene expression between the two sexes, most genes from the male X chromosome are hyperactivated by a special dosage compensation system. Dosage compensation is achieved by a complex of at least six proteins and two noncoding RNAs that specifically associate with the male X. A central question is how the X chromosome is recognized. According to a current model, complexes initially assemble at approximately 35 chromatin entry sites on the X and then spread bidirectionally along the chromosome where they occupy hundreds of sites. Here, we report that mutations in Trithorax-like (Trl) lead to the loss of a single chromatin entry site on the X, male lethality, and mislocalization of dosage compensation complexes.

Animals↗
PubMed2004

Evidence for a piwi-dependent RNA silencing of the gypsy endogenous retrovirus by the Drosophila melanogaster flamenco gene.

In Drosophila melanogaster, the endogenous retrovirus gypsy is repressed by the functional alleles (restrictive) of an as-yet-uncloned heterochromatic gene called flamenco. Using gypsy-lacZ transcriptional fusions, we show here that this repression takes place not only in the follicle cells of restrictive ovaries, as was previously observed, but also in restrictive larval female gonads. Analyses of the role of gypsy cis-regulatory sequences in the control of gypsy expression are also presented. They rule out the hypothesis that gypsy would contain a single binding region for a putative Flamenco repressor. Indeed, the ovarian expression of a chimeric yp3-lacZ construct was shown to become sensitive to the Flamenco regulation when any of three different 5'-UTR gypsy sequences (ranging from 59 to 647 nucleotides) was incorporated into the heterologous yp3-lacZ transcript. The piwi mutation, which is known to affect RNA-mediated homology-dependent transgene silencing, was also shown to impede the repression of gypsy in restrictive female gonads. Finally, a RNA-silencing model is also supported by the finding in ovaries of short RNAs (25-27 nucleotides long) homologous to sequences from within the gypsy 5'-UTR.

5' Untranslated Regions↗
PubMed2001

Resistance to Bacillus sphaericus in Culex pipiens (Diptera: Culicidae): interaction between recessive mutants and evolution in southern France.

In southern France, failure to control Culex pipiens L. with Bacillus sphaericus Neide toxin (Bs) was first detected in 1994, at the extreme east of the Languedoc-Roussillon coast. This failure was due to a single recessive mutant, sp-1R. Two complementary strategies were used to test whether sp-1R had invaded the Bs-controlled area by 1998. First, a strain (BP) was selected from resistant larvae sampled in the western part of the Bs-controlled area. In BP strain, resistance involved a single recessive gene, sp-2R, distinct from sp-1R, that conferred a similarly high resistance in the homozygous state (approximately 6,000-fold). Combining one copy of sp-1R and one of sp-2R conferred a > 100-fold resistance. Second, Bs-resistance was monitored among the offspring of field females crossed to sp-1RR homozygous males. Females were sampled in 20 localities of southern France and three localities of the Llobregat delta (Barcelona, Spain) where C. pipiens control is also intensive. The 537 females in the study produced enough larvae to infer their genotype: 462 progenies were susceptible and the survival rate of 51 others was explained by the presence of sp-1R and/or sp-2R. The remaining 24 cases indicated that other factors could confer resistance when combined with sp-1R. The current data showed that, even when recessive, resistant mutants can rapidly increase in frequency, providing some interactions that protect them from disappearance. We discuss the consequences of this finding on the current strategies aimed to avoid or delay resistance in the pests controlled with B. sphaericus or B. thuringiensis Berliner toxins.

Animals↗
PubMed2001

A single gene (yes) controls pigmentation of eyes and scales in Heliothis virescens.

A yellow-eyed mutant was discovered in a strain of Heliothis virescens, the tobacco budworm, that already exhibited a mutation for yellow scale, y. We investigated the inheritance of these visible mutations as candidate markers for transgenesis. Yellow eye was controlled by a single, recessive, autosomal factor, the same type of inheritance previously known for y. Presence of the recombinant mutants with yellow scales and wild type eyes in test crosses indicated independent segregation of genes for these traits. The recombinant class with wild type scales and yellow eyes was completely absent and there was a corresponding increase of the double mutant parental class having yellow scales and yellow eyes. These results indicated that a single factor for yellow eye also controlled yellow scales independently of y. This gene was named yes, for yellow eye and scale. We hypothesize that yes controls both eye and scale color through a deficiency in transport of pigment precursors in both the ommochrome and melanin pathways. The unlinked gene y likely controls an enzyme affecting the melanin pathway only. Both y and yes segregated independently of AceIn, acetylcholinesterase insensitivity, and sodium channel hscp, which are genes related to insecticide resistance.

Acetylcholinesterase↗
PubMed1997

Mutations induced in Drosophila during space flight.

To examine the possible effects of space radiation on living organisms, fruit flies Drosophila melanogaster were loaded on the US Space Shuttle Endeavour, and after the flight we have analyzed two types of mutations, sex-linked recessive lethal mutations induced in male reproductive cells and somatic mutations which give rise to morphological changes in hairs growing on the surface of wing epidermal cells. Wild type strains and a radiation-sensitive strain mei-41 were used. The frequencies of sex-linked recessive lethal mutations in flight groups were 2 and 3 times higher for wild type Canton-S and mei-41 strains, respectively, than those in ground control groups. By contrast, the frequencies of wing-hair somatic mutations differed little between flight and control groups. The possibility that the space environment causes mutations in certain types of cells such as male reproductive cells, is discussed.

Animals↗