TheVestigialGene ofDrosophila Melanogasteris Involved in the Formation of the Peripheral Nervous System: Genetic Interactions with theScute Gene

Zider, Alain; Paumard-Rigal, Solange; Frouin, Isabelle; Silber, Joël

doi:10.3109/01677069809167258

Cited by 10 publications

(7 citation statements)

References 19 publications

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“…Some of the male lethal events also caused a scalloped-wing phenotype in heterozygous females. For those that did not, testing to ensure that the male lethality was due to deletion of scalloped coding sequence was performed by recovering the repaired chromosomes in trans to the hypomorphic sd 1 mutation [79] and scoring for a scalloped-wing phenotype. Repair events which could be recovered in males were subjected to PCR analysis, using primers internal to P(w a } [43], to detect small deletions into one or both introns of sd .…”

Section: Methodsmentioning

confidence: 99%

Dual Roles for DNA Polymerase Theta in Alternative End-Joining Repair of Double-Strand Breaks in Drosophila

2010

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DNA double-strand breaks are repaired by multiple mechanisms that are roughly grouped into the categories of homology-directed repair and non-homologous end joining. End-joining repair can be further classified as either classical non-homologous end joining, which requires DNA ligase 4, or “alternative” end joining, which does not. Alternative end joining has been associated with genomic deletions and translocations, but its molecular mechanism(s) are largely uncharacterized. Here, we report that Drosophila melanogaster DNA polymerase theta (pol theta), encoded by the mus308 gene and previously implicated in DNA interstrand crosslink repair, plays a crucial role in DNA ligase 4-independent alternative end joining. In the absence of pol theta, end joining is impaired and residual repair often creates large deletions flanking the break site. Analysis of break repair junctions from flies with mus308 separation-of-function alleles suggests that pol theta promotes the use of long microhomologies during alternative end joining and increases the likelihood of complex insertion events. Our results establish pol theta as a key protein in alternative end joining in Drosophila and suggest a potential mechanistic link between alternative end joining and interstrand crosslink repair.

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Section: Methodsmentioning

confidence: 99%

Dual Roles for DNA Polymerase Theta in Alternative End-Joining Repair of Double-Strand Breaks in Drosophila

2010

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“…Vgl-2 Protein Translocates from the Cytoplasm to the Nucleus upon Muscle Differentiation-In Drosophila, Vestigial is a nuclear protein (34). We constructed a myc-tagged mouse Vgl- 2 FIG.…”

Section: Vgl-2 a Muscle-specific Cofactor Of Tef-1 And Mef2mentioning

confidence: 99%

Mammalian Vestigial-like 2, a Cofactor of TEF-1 and MEF2 Transcription Factors That Promotes Skeletal Muscle Differentiation

Maeda¹,

Chapman²,

Stewart³

2002

Journal of Biological Chemistry

169

176

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Expression of many skeletal muscle-specific genes depends on TEF-1 (transcription enhancer factor-1) and MEF2 transcription factors. In Drosophila, the TEF-1 homolog Scalloped interacts with the cofactor Vestigial to drive differentiation of the wing and indirect flight muscles. Here, we identify three mammalian vestigiallike genes, Vgl-1, Vgl-2, and Vgl-3, that share homology in a TEF-1 interaction domain. Vgl-1 and Vgl-3 transcripts are enriched in the placenta, whereas Vgl-2 is expressed in the differentiating somites and branchial arches during embryogenesis and is skeletal musclespecific in the adult. During muscle differentiation, Vgl-2 mRNA levels increase and Vgl-2 protein translocates from the cytoplasm to the nucleus. In situ hybridization revealed co-expression of Vgl-2 with myogenin in the differentiating muscle of embryonic myotomes but not in newly formed somites prior to muscle differentiation. Like Vgl-1, Vgl-2 interacts with TEF-1. In addition, we show that Vgl-2 interacts with MEF2 in a mammalian two-hybrid assay and that Vgl-2 selectively binds to MEF2 in vitro. Co-expression of Vgl-2 with MEF2 markedly co-activates an MEF2-dependent promoter through its MEF2 element. Overexpression of Vgl-2 in MyoDtransfected 10T 1 ⁄2 cells markedly increased myosin heavy chain expression, a marker of terminal muscle differentiation. These results identify Vgl-2 as an important new component of the myogenic program.Commitment of pluripotent cells to the skeletal muscle lineage involves multiple inductive signals and the hierarchical activation of several transcription factors (1). Differentiation of skeletal muscle cells is coupled to withdrawal from the cell cycle and is accompanied by transcriptional activation of muscle-specific genes. The MyoD family of basic-helix-loop-helix transcription factors, including MyoD, Myf5, myogenin, and MRF4, plays a central role in activating the muscle differentiation program (2). Activation of muscle gene expression by the MyoD family of factors is dependent on their association with members of the MEF2 family of MADS box transcription factors (3). Together, MyoD and MEF2 account for a large part of muscle-specific gene activation. In addition, many muscle genes contain muscle-specific cytidine-adenosine-thymidine cis-elements (5Ј-CATDSH-3Ј) that are also required for musclespecific expression (4, 5). The proteins that bind to these elements belong to the transcription enhancer factor-1 (TEF-1)

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“…A complete absence of wing structures is observed in vg null homozygotes (Paumard‐Rigal et al . 1998; Zider et al . 1998).…”

Section: Introductionmentioning

confidence: 99%

Cell cycle genes regulate vestigial and scalloped to ensure normal proliferation in the wing disc of Drosophila melanogaster

Legent¹,

Dutriaux²,

Delanoue³

et al. 2006

Genes to Cells

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In Drosophila , the Vestigial-Scalloped (VG-SD) dimeric transcription factor is required for wing cell identity and proliferation. Previous results have shown that VG-SD controls expression of the cell cycle positive regulator dE2F1 during wing development. Since wing disc growth is a homeostatic process, we investigated the possibility that genes involved in cell cycle progression regulate vg and sd expression in feedback loops. We focused our experiments on two major regulators of cell cycle progression: dE2F1 and the antagonist dacapo ( dap ). Our results reinforce the idea that VG/SD stoichiometry is critical for correct development and that an excess in SD over VG disrupts wing growth. We reveal that transcriptional activity of VG-SD and the VG/SD ratio are both modulated by down-expression of cell cycle genes. We also detected a dap -induced sd up-regulation that disrupts wing growth. Moreover, we observed a rescue of a vg hypomorphic mutant phenotype by dE2F1 that is concomitant with vg and sd induction. This regulation of the VG-SD activity by dE2F1 is dependent on the vg genetic background. Our results support the hypothesis that cell cycle genes fine-tune wing growth and cell proliferation, in part, through control of the VG/SD stoichiometry and activity. This points to a homeostatic feedback regulation between proliferation regulators and the VG-SD wing selector. IntroductionCell proliferation is a complex process that requires the activity of the genes involved in cell cycle progression, DNA replication and mitosis. Previous work has provided evidence that differentiation or patterning genes directly control cell cycle gene expression (DumanScheel et al . 2002;Hwang et al . 2002). Conversely, proliferation signals also regulate various differentiation pathways (Muller et al . 2001;Dimova et al . 2003).The Drosophila wing imaginal disc provides a powerful model for investigating the pathways that connect growth, proliferation and patterning during development (Neufeld et al . 1998). Genes of the E2F family are the main regulators of proliferation and cell cycle control (Harbour & Dean 2000). The binding of dE2F1 to the DP subunit provides a heterodimeric transcription factor whose target genes ensure the G1/S transition (Ohtani & Nevins 1994;Duronio et al . 1995). During the G1 phase, expression of these genes is repressed by the binding of the RBF-related pocket proteins (Retinoblastoma Family) to dE2F1. At late G1, RBF phosphorylation by Cyclin-CDK complexes releases free dE2F1-DP which up-regulates genes involved in the DNA replication machinery as well as cell cycle progression (Du et al . 1996). In Drosophila , the Cyclin-dependent Kinase Inhibitor (CKI) dacapo ( dap , a p21 CIP1 homolog) inhibits the core cell cycle machinery through the binding and down-regulation of Cyclin-CDK enzymatic activities. This restriction of the G1/S transition often accompanies the switch from proliferation to differentiation (Lane et al . 1996;de Nooij et al . 1996). Recently, reports identified respective feedback...

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TheVestigialGene ofDrosophila Melanogasteris Involved in the Formation of the Peripheral Nervous System: Genetic Interactions with theScute Gene

Cited by 10 publications

References 19 publications

Dual Roles for DNA Polymerase Theta in Alternative End-Joining Repair of Double-Strand Breaks in Drosophila

Dual Roles for DNA Polymerase Theta in Alternative End-Joining Repair of Double-Strand Breaks in Drosophila

Mammalian Vestigial-like 2, a Cofactor of TEF-1 and MEF2 Transcription Factors That Promotes Skeletal Muscle Differentiation

Cell cycle genes regulate vestigial and scalloped to ensure normal proliferation in the wing disc of Drosophila melanogaster

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