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PubMed1998

shaven and sparkling are mutations in separate enhancers of the Drosophila Pax2 homolog.

We have previously shown that the sparkling gene, which like mammalian Pax2 plays an important role in eye development, is encoded by the Drosophila homolog of Pax2. Here we demonstrate that D-Pax2 also encodes the shaven function, which is crucial during bristle development. Both sv and spa alleles, previously thought to represent different genes, are mutations in two widely separated enhancers of D-Pax2. The sv function of D-Pax2 acts in at least two distinct steps of mechanosensory bristle development: the specification of the alternative fate of shaft as opposed to socket cell, and later the differentiation of the shaft cell.

Alleles↗
PubMed1998

Functional dominance among Hox genes: repression dominates activation in the regulation of Dpp.

Here we investigate the mechanisms by which Hox genes compete for the control of positional identity. Functional dominance is often observed where different Hox genes are co-expressed, and frequently the more posteriorly expressed Hox gene is the one that prevails, a phenomenon known as posterior prevalence. We use dpp674, a visceral mesoderm-specific enhancer of decapentaplegic (dpp), to investigate functional dominance among Hox genes molecularly. We find that posterior prevalence does not adequately describe the regulation of dpp by Hox genes. Instead, we find that abdominal-A (abd-A) dominates over the more posterior Abdominal-B (Abd-B) and the more anterior Ultrabithorax (Ubx). In the context of the dpp674 enhancer, abd-A functions as a repressor whereas Ubx and Abd-B function as activators. Thus, these results suggest that other cases of Hox competition and functional dominance may also be understood in terms of competition for target gene regulation in which repression dominates over activation.

Animals↗
PubMed1998

The Drosophila Medea gene is required downstream of dpp and encodes a functional homolog of human Smad4.

The Transforming Growth Factor-beta superfamily member decapentaplegic (dpp) acts as an extracellular morphogen to pattern the embryonic ectoderm of the Drosophila embryo. To identify components of the dpp signaling pathway, we screened for mutations that act as dominant maternal enhancers of a weak allele of the dpp target gene zerknŁllt. In this screen, we recovered new alleles of the Mothers against dpp (Mad) and Medea genes. Phenotypic analysis of the new Medea mutations indicates that Medea, like Mad, is required for both embryonic and imaginal disc patterning. Genetic analysis suggests that Medea may have two independently mutable functions in patterning the embryonic ectoderm. Complete elimination of maternal and zygotic Medea activity in the early embryo results in a ventralized phenotype identical to that of null dpp mutants, indicating that Medea is required for all dpp-dependent signaling in embryonic dorsal-ventral patterning. Injection of mRNAs encoding DPP or a constitutively activated form of the DPP receptor, Thick veins, into embryos lacking all Medea activity failed to induce formation of any dorsal cell fates, demonstrating that Medea acts downstream of the thick veins receptor. We cloned Medea and found that it encodes a protein with striking sequence similarity to human SMAD4. Moreover, injection of human SMAD4 mRNA into embryos lacking all Medea activity conferred phenotypic rescue of the dorsal-ventral pattern, demonstrating conservation of function between the two gene products.

Amino Acid Sequence↗
PubMed2000

Generation of medial and lateral dorsal body domains by the pannier gene of Drosophila.

The pannier (pnr) gene encodes a GATA transcription factor and acts in several developmental processes in Drosophila, including embryonic dorsal closure, specification of cardiac cells and bristle determination. We show that pnr is expressed in the mediodorsal parts of thoracic and abdominal segments of embryos, larvae and adult flies. Its activity confers cells with specific adhesion properties that make them immiscible with non-expressing cells. Thus there are two genetic domains in the dorsal region of each segment: a medial (MED) region where pnr is expressed and a lateral (LAT) region where it is not. The homeobox gene iroquois (iro) is expressed in the LAT region. These regions are not formed by separate polyclones of cells, but are defined topographically. We show that ectopic pnr in the wing induces MED thoracic development, indicating that pnr specifies the identity of the MED regions. Correspondingly, when pnr is removed from clones of cells in the MED domain, they sort out and apparently adopt the LAT fate. We propose that (1) the subdivision into MED and LAT regions is a general feature of the Drosophila body plan and (2) pnr is the principal gene responsible for this subdivision. We argue that pnr acts like a classical selector gene but differs in that its expression is not propagated through cell divisions.

Abdomen↗
PubMed2000

Methylation and expression of amplified esterase genes in the aphid Myzus persicae (Sulzer).

Most populations of the aphid Myzus persicae have amplified genes (up to 80 copies) encoding the insecticide-detoxifying esterase E4. This paper reports the analysis of methylation of the E4 gene and its flanking DNA with the use of methylation-sensitive restriction enzymes, CpG profiling and bisulphite sequencing. In combination these show that E4 has 5-methylcytosine confined to CpG doublets, as previously shown for vertebrate genomes; this is the first such report for an insect gene. The methylation is present within the gene but absent from upstream regions, including the 5' CpG-rich region around the start of transcription, and from 3' flanking DNA. Methylated E4 genes are expressed; loss of the 5-methylcytosine is correlated with a loss of transcription, although this is not accompanied by a global loss of the 5-methylcytosine present in the aphid genome. These results suggest that the methylation of E4 has a positive role in expression, and call into question the widely held view that methylation in invertebrate genomes is confined to regions that do not contain genes and that methylation is always associated with gene silencing.

Animals↗
PubMed1996

Engrailed gene dosage determines whether certain recessive cubitus interruptus alleles exhibit dominance of the adult wing phenotype in Drosophila.

The cubitus interruptus (ci) locus of Drosophila melanogaster is needed for normal development. Some mutants of this gene result in embryonic lethality, while others just disrupt adult wing veins. While undertaking a genetic screen for additional ci mutations that affect the wing veins, we recovered a modifier mutation on chromosome two that produced a ci phenotype in recessive ci heterozygotes (ci(recessive)/+). We identified the modifier mutation as an allele of engrailed and have called it engrailed-enhancer of cubitus interruptus (enEnci). As a double heterozygote (en-/+; ci-/+) this new en allele dominantly generates a ci wing vein phenotype. As a double heterozygote, it also enhances the ci wing vein phenotype of the dominant alleles ciW and ciCe2, but not ciD. Other loss-of-function en alleles also enhance the ci phenotype, with the en lethal alleles (and deletions) showing the strongest effect, while the homozygous viable en alleles show weaker enhancement. Strong en- alleles failed to induce a ci phenotype with heterozygotes of ci recessive lethal alleles l(4)13, l(4)17, or ciDrev, which are loss-of-function mutations. This supports a previous proposal that the ci wing vein phenotype is not due to loss of ci+ function, as would be expected for most recessive alleles. Instead, the adult wing vein abnormality is due to ectopic expression (or de-repression) of the ci transcript in the posterior compartment of the wing disc. We also observed that en-/+ heterozygotes could induce a ci phenotype in situations where the ci+ locus is either unpaired or hemizygous. Since loss of one en+ gene dose enhanced the ci phenotype, three doses of en+ were tested and found to suppress expression of the ci phenotype in ci1 homozygotes and ciW heterozygotes. These observations show that correct regulation of the ci gene involves more than the simple interaction of upstream regulatory elements. some pairing, pairing dependent gene repression, position effects.

Alleles↗
PubMed1997

IMP-L3, A 20-hydroxyecdysone-responsive gene encodes Drosophila lactate dehydrogenase: structural characterization and developmental studies.

IMP-L3, a gene isolated as a potential mediator of imaginal disc morphogenesis in Drosophila melanogaster, encodes lactate dehydrogenase (LDH). The predicted amino acid sequence of IMP-L3 is 58-61% identical to those of human LDHs. In cultured imaginal discs, IMP-L3 transcript levels and LDH enzyme activity increase in response to the steroid hormone, 20-hydroxyecdysone. In embryos, IMP-L3 transcript and LDH activity appear in developing somatic muscles by late stage 13, well before the onset of muscular contraction. High levels of transcript and LDH activity persist throughout embryogenesis and throughout larval development. The gene has been localized by in situ hybridization and deficiency mapping to 65A7-65B2 on the third chromosome. LDH activity is reduced to approximately 50% of wild type in animals heterozygous for a deficiency that removes the 65A-B region. Embryos deficient for the 65A-b region lack LDH activity. We conclude that IMP-L3 is the only gene that encodes LDH in Drosophila.

Amino Acid Sequence↗
PubMed1997

Control of early neurogenesis of the Drosophila brain by the head gap genes tll, otd, ems, and btd.

The progenitors of the Drosophila central nervous system (CNS), called neuroblasts, segregate from the neurectoderm of the early embryo in a stereotyped pattern. The neuroblasts that give rise to the brain segregate from the procephalic neurectoderm and form three neuromeres, called protocerebrum, deuterocerebrum, and tritocerebrum. The expression of the proneural genes of the achaete-scute complex (AS-C) is required for neurectodermal cells to acquire the competency to form neuroblasts. We show here that the expression of the proneural gene lethal of scute (l'sc) is required for the development of the majority of the procephalic neuroblasts. l'sc expression in the procephalic neurectoderm is controlled by the head gap genes tailless (tll), orthodenticle (otd), buttonhead (btd), and empty spiracles (ems), which are expressed in partially overlapping domains of the head neurectoderm. Loss of function of a given head gap gene results in the absence of l'sc expression in its domain, followed by the absence of neuroblasts that would normally segregate from this domain. Loss of tll function results in the absence of all protocerebral neuroblasts, otd functions in a domain that includes a large part of the protocerebrum and a smaller part of the adjacent deuterocerebrum. Both ems and btd are required in partially overlapping subsets of neuroblasts of the deuterocerebrum and tritocerebrum.

Animals↗
PubMed2001

Construction of a recombinant Anticarsia gemmatalis nucleopolyhedrovirus (AgMNPV-2D) harbouring the beta-galactosidase gene.

We have constructed a transfer vector (pAgGal) containing the beta-galactosidase gene under control of the Escherichia coli gpt and AgMNPV polyhedrin (polh) promoters. The transfer vector was cotransfected with wild type Anticarsia gemmatalis nucleopolyhedrovirus (AgMNPV) DNA into A. gemmatalis (UFL-AG-286) cells and a recombinant baculovirus (vAgGalA2) was isolated. The beta-galactosidase gene insertion was checked by polymerase chain reaction (PCR) using DNA from AgMNPV and vAgGalA2 and primers specific for regions upstream and downstream of the polh gene. Insect cells (UFL-AG-286) were infected with the recombinant vAgGalA2 and wild type AgMNPV viruses and the production of the heterologous protein analyzed by SDS-PAGE and Pulse-Chase. Beta-galactosidase was expressed at high levels late on infection as expected for a gene under the control of the polh promoter. The highly expressed beta-galactosidase protein was also shown to be biologically active by a beta-galactosidase assay.

Animals↗
PubMed1996

Three mutant genes cooperatively induce brain tumor formation in Drosophila malignant brain tumor.

The Drosophila melanogaster strain Malignant Brain Tumor reveals temperature-sensitive transformation of the larval brain tissue. Genetic analysis shows that three gene defects, spzMBT, yetiMBT, and tldMBT, cooperatively induce brain tumor formation. Whereas spz and tld belong to the genes inducing differentiation patterns in the embryo, yeti induces cell overgrowth. spzMBT-, yetiMBT-, and tldMBT-containing animals are larval lethal, whereas Malignant Brain Tumor is kept as a homozygous strain at a permissive temperature. This reveals that this tumor-forming strain is the result of a number of adaptive mutation events.

Animals↗
PubMed2000

An autoregulatory function of Dfos during Drosophila endoderm induction.

The endoderm of Drosophila is patterned during embryogenesis by an inductive cascade emanating from the adhering mesoderm. An immediate-early endodermal target gene of this induction is Dfos whose expression is upregulated in the middle midgut by Dpp signalling. Previous evidence based on a dominant-negative Dfos construct indicated that Dfos may cooperate with Dpp signalling to induce the HOX gene labial, the ultimate target gene of the inductive cascade. Here, we examine kayak mutants that lack Dfos to establish that Dfos is indeed required for labial induction. We provide evidence that Dfos acts through a CRE-like sequence, previously identified to be a target for signalling by Dpp and by the Epidermal growth factor receptor (Egfr) in the embryonic midgut. We show that Dfos expression is stimulated by Egfr signalling. Finally, we find that Dfos function is required for its own upregulation. Thus, endoderm induction is based on at least four tiers of positive autoregulatory feedback loops.

Animals↗
PubMed1999

The pioneer gene, apontic, is required for morphogenesis and function of the Drosophila heart.

In an effort to isolate genes required for heart development and to further our understanding of cardiac specification at the molecular level, we screened PlacZ enhancer trap lines for expression in the Drosophila heart. One of the lines generated in this screen, designated B2-2-15, was particularly interesting because of its early pattern of expression in cardiac precursor cells, which is dependent on the homeobox gene tinman, a key determinant of heart development in Drosophila. We isolated and characterized a gene in the vicinity of B2-2-15 that exhibits an identical expression pattern than the reporter gene of the enhancer trap. The product of his gene, apontic (apt; see also "Gellon et al., 1997"), does not appear to have any homology with known genes. apt mutant embryos show distinct abnormalities in heart morphology as early as mid-embryonic stages when the heart tube assembles, in that segments of heart cells (those of myocardial and pericardial identity) are often missing. Most strikingly, however, apt mutant embryos or larvae only develop a much reduced heart rate, perhaps because of defects in the assembly of an intact heart tube and/or because of defects in the function or physiological control of the myocardial cells, which normally mediate heart contractions. These cardiac defects may be the cause of death of these mutants during late embryonic or early larval stages.

Alleles↗
PubMed1999

The Drosophila ATM homologue Mei-41 has an essential checkpoint function at the midblastula transition.

BACKGROUND: Drosophila embryogenesis is initiated by 13 rapid syncytial mitotic divisions that do not require zygotic gene activity. This maternally directed cleavage phase of development terminates at the midblastula transition (MBT), at which point the cell cycle slows dramatically, membranes surround the cortical nuclei to form a cellular blastoderm, and zygotic gene expression is first required. RESULTS: We show that embryos lacking Mei-41, a Drosophila homologue of the ATM tumor suppressor, proceed through unusually short syncytial mitoses, fail to terminate syncytial division following mitosis 13, and degenerate without forming cells. A similar cleavage-stage arrest is produced by mutations in grapes, which encodes a homologue of the Checkpoint-1 kinase. We present biochemical, cytological and genetic data indicating that Mei-41 and Grapes are components of a conserved DNA-replication/damage checkpoint pathway that triggers inhibitory phosphorylation of the Cdc2 kinase and mediates resistance to replication inhibitors and DNA-damaging agents. This pathway is nonessential during postembryonic development, but it is required to terminate the cleavage stage at the MBT. Cyclins are required for Cdc2 kinase activity, and mutations in cyclin A and cyclin B bypass the requirement for mei-41 at the MBT. These mutations do not restore wild-type syncytial cell-cycle timing or the embryonic replication checkpoint, however, suggesting that Mei-41-mediated inhibition of Cdc2 has an additional essential function at the MBT. CONCLUSIONS: The Drosophila DNA-replication/damage checkpoint pathway can be activated by externally triggered DNA damage or replication defects throughout the life cycle, and under laboratory conditions this inducible function is nonessential. During early embryogenesis, however, this pathway is activated by developmental cues and is required for the transition from maternal to zygotic control of development at the MBT.

Animals↗
PubMed1998

Tout-velu is a Drosophila homologue of the putative tumour suppressor EXT-1 and is needed for Hh diffusion.

Hedgehog (Hh) proteins act through both short-range and long-range signalling to pattern tissues during invertebrate and vertebrate development. The mechanisms allowing Hedgehog to diffuse over a long distance and to exert its long-range effects are not understood. Here we identify a new Drosophila gene, named tout-velu, that is required for diffusion of Hedgehog. Characterization of tout-velu shows that it encodes an integral membrane protein that belongs to the EXT gene family. Members of this family are involved in the human multiple exostoses syndrome, which affects bone morphogenesis. Our results, together with the previous characterization of the role of Indian Hedgehog in bone morphogenesis, lead us to propose that the multiple exostoses syndrome is associated with abnormal diffusion of Hedgehog proteins. These results show the existence of a new conserved mechanism required for diffusion of Hedgehog.

Amino Acid Sequence↗
PubMed1997

A steroid-triggered switch in E74 transcription factor isoforms regulates the timing of secondary-response gene expression.

The steroid hormone 20-hydroxyecdysone (referred to here as ecdysone) directs Drosophila metamorphosis by activating a series of genetic regulatory hierarchies. ETS domain transcription factors encoded by the ecdysone-inducible E74 early gene, E74A and E74B, act at the top of these hierarchies to coordinate the induction of target genes. We have ectopically expressed these E74 isoforms to understand their regulatory functions during the onset of metamorphosis. We show that E74 can regulate its own transcription, most likely through binding sites within its gene. Ectopic expression of E74B can partially repress the E78B and DHR3 orphan receptor genes, suggesting a role for E74 in the appropriate timing of early-late gene expression. Furthermore, E74A is both necessary and sufficient for E78B induction, implicating E74A as a key regulator of E78B expression. We also show, consistent with our studies of E74 loss-of-function mutations, that E74B is a potent repressor of late gene transcription and E74A is sufficient to prematurely induce the L71-1 late gene. However, ectopic expression of both Broad-Complex and E74A activators in an E74B mutant background is not sufficient to prematurely induce all late genes, indicating that other factors contribute to this regulatory circuit. These observations demonstrate that the steroid-triggered switch in E74 transcription factor isoforms plays a central role in the proper timing of secondary-response gene expression.

Animals↗
PubMed1998

Drosophila CtBP: a Hairy-interacting protein required for embryonic segmentation and hairy-mediated transcriptional repression.

hairy is a Drosophila pair-rule segmentation gene that functions genetically as a repressor. To isolate protein components of Hairy-mediated repression, we used a yeast interaction screen and identified a Hairy-interacting protein, the Drosophila homolog of the human C-terminal-binding protein (CtBP). Human CtBP is a cellular phosphoprotein that interacts with the C-terminus of the adenovirus E1a oncoprotein and functions as a tumor suppressor. dCtBP also interacts with E1a in a directed yeast two-hybrid assay. We show that dCtBP interacts specifically and directly with a small, previously uncharacterized C-terminal region of Hairy. dCtBP activity appears to be specific to Hairy of the Hairy/Enhancer of split [E(spl)]/Dpn basic helix-loop-helix protein class. We identified a P-element insertion within the dCtBP transcription unit that fails to complement alleles of a known locus, l(3)87De. We demonstrate that dCtBP is essential for proper embryonic segmentation by analyzing embryos lacking maternal dCtBP activity. While Hairy is probably not the only segmentation gene interacting with dCtBP, we show dose-sensitive genetic interactions between dCtBP and hairy mutations.

Adenovirus E1A Proteins↗
PubMed1995

Drawing a stripe in Drosophila imaginal disks: negative regulation of decapentaplegic and patched expression by engrailed.

During development of the Drosophila adult appendage precursors, the larval imaginal disks, the decapentaplegic (dpp) gene is expressed in a stripe just anterior to the anterior/posterior (A/P) compartment boundary. Here, we investigate the genetic controls that lead to production of this stripe. We extend previous observations on leaky engrailed (en) mutations by showing that mutant clones completely lacking both en and invected (inv) activity ectopically express dpp-lacZ reporter genes in the posterior compartment, where dpp activity ordinarily is repressed. Similarly, patched (ptc) is also ectopically expressed in such posterior compartment en-inv- null clones. In contrast, these en-inv- clones exhibit loss of hedgehog (hh) expression. We suggest that the absence of dpp expression in the posterior compartment is due to direct repression by en. Ubiquitious expression of en in imaginal disks, produced by a hs-en construct, eliminates the expression of dpp-lacZ in its normal A/P boundary stripe. We identify three in vitro Engrailed binding sites in one of our dpp-lacZ reporter gene. Mutagenesis of these Engrailed binding sites results in ectopic expression of this reporter gene, but does not alter the normal stripe of expression at the A/P boundary. We propose that the en-hh-ptc regulatory loop that is responsible for segmental expression of wingless in the embryo is reutilized in imaginal disks to create a stripe of dpp expression along the A/P compartment boundary.

Animals↗
PubMed1997

oroshigane, a new segment polarity gene of Drosophila melanogaster, functions in hedgehog signal transduction.

Here we describe a new segment polarity gene of Drosophila melanogaster, oroshigane (oro). Identified as a dominant enhancer of Bar (B), oro is also recessive embryonic lethal, and homozygous oro embryos show variable substitution of naked cuticle with denticles. These patterns are distinctly similar to those of hedgehog (hh) and wingless (wg) embryos, which indicates that oro functions in determining embryonic segment polarity. Evidence that oro function is involved in Hh signal transduction during embryogenesis is provided by its genetic interactions with the segment polarity genes patched (ptc) and fused (fu). Furthermore, ptcIN is a dominant suppressor of the oro embryonic lethal phenotype, suggesting a close and dose-dependent relationship between oro and ptc in Hh signal transduction. oro function is also required in imaginal development. The oroI allele significantly reduces decapentaplegic (dpp), but not hh, expression in the eye imaginal disc. Furthermore, oro enhances the fui wing phenotype in a dominant manner. Based upon the interactions of oro with hh, ptc, and fu, we propose that the oro gene plays important roles in Hh signal transduction.

Animals↗