Different mechanisms initiate and maintain<i>wingless</i>expression in the<i>Drosophila</i>wing hinge

Rodrı́guez, David del Álamo; Terriente, Javier; Galindo, Máximo Ibo; Couso, Juan Pablo; Díaz-Benjumea, Fernando J.

doi:10.1242/dev.129.17.3995

Cited by 36 publications

(9 citation statements)

References 51 publications

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“…Several other well-known wing development TFs were identified, including tailup and odd-paired in the notum, ultrabithorax and C15 in the peripodial epithelium and twist in the myoblasts (Figure 2.c-d, Supplementary Figure 3.a-c). Another interesting example is nubbin ( nub ), a POU/homeodomain transcription factor targeted by vestigial (Rodríguez et al, 2002), which is found specifically expressed in the pouch domain (Supplementary Figure 3.a). An extended list of TFs and their target genes can be queried via SCope (https://scope.aertslab.org/#/WingAtlas/*/welcome), and is provided as a Supplementary Table 2.…”

Section: Resultsmentioning

confidence: 99%

Shared enhancer gene regulatory networks between wound and oncogenic programs

Floc’hlay

Balaji

Christiaens

et al. 2022

Preprint

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Wound response programs are often activated during neoplastic growth in tumors. In both wound repair and tumor growth, cells respond to acute stress and balance the activation of multiple programs including apoptosis, proliferation, and cell migration. Central to those responses are the activation of the JNK/MAPK and JAK/STAT signaling pathways. Yet, to what extent these signaling cascades interact at the cis-regulatory level, and how they orchestrate different regulatory and phenotypic responses is still unclear. Here, we aim to characterize the regulatory states that emerge and cooperate in the wound response, using the Drosophila melanogaster wing disc as a model system, and compare these with cancer cell states induced by rasV12scrib-/- in the eye disc. We used single-cell multiome profiling to derive enhancer Gene Regulatory Networks (eGRNs) by integrating chromatin accessibility and gene expression signals. We identify a proliferative eGRN, active in the majority of wounded cells and controlled by AP-1 and STAT. In a smaller, but distinct population of wound cells, a senescent eGRN is activated and driven by C/EBP-like transcription factors (Irbp18, Xrp1, Slow border, and Vrille) and Scalloped. In tumor cells on the other hand, both eGRN signatures are simultaneously active within the same cell. Our single-cell multiome and eGRNs resource offers an in-depth characterisation of the senescence markers, together with a new perspective on the shared gene regulatory programs acting during wound response and oncogenesis.

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Section: Resultsmentioning

confidence: 99%

Shared enhancer gene regulatory networks between wound and oncogenic programs

Floc’hlay

Balaji

Christiaens

et al. 2022

Preprint

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“…The larval expression of wg begins at the second instar (48 h after egg laying, AEL) in a ventral anterior region of the wing discs 26 directed by a well characterized early enhancer 27 . In early third instar larvae, the expression of wg is detectable in the D/V boundary and the IR 7 , 27 (Fig. 5 A).…”

Section: Resultsmentioning

confidence: 98%

“…Different regulators control the expression of wg to define the boundaries and domains on the wing disc 7 , 8 . In the late third instar wing disc, wg is expressed in a broad band located at the notum, along the D/V boundary, and in two concentric ring-like patterns at the hinge region called the inner (IR) and the outer (OR) ring domains 9 (Fig.…”

Section: Introductionmentioning

confidence: 99%

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TnaA, a trithorax group protein, modulates wingless expression in different regions of the Drosophila wing imaginal disc

Rosales-Vega,

Reséndez-Pérez,

Zurita

et al. 2023

Sci Rep

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Abstractwingless expression is exquisitely regulated by different factors and enhancers in the imaginal wing discs of Drosophila melanogaster in four domains: the dorsal band, the dorso-ventral boundary, and the inner and outer ring domains. tonalli is a trithorax group gene that encodes a putative SUMO E3 ligase that binds to chromatin to regulate the expression of its targets, including the Hox genes. However, its role in modulating gene expression is barely known. Here, we show that TnaA modulates the wingless expression at two domains of the wing disc, the dorso-ventral boundary and the inner ring. At first, tonalli interacts genetically with Notch to form the wing margin. In the inner ring domain, TnaA modulates wingless transcription. When the dosage of TnaA increases in or near the inner ring since early larval stages, this domain expands with a rapid increase in wingless expression. TnaA occupies the wingless Inner Ring Enhancer at the wing disc, meanwhile it does not affect wingless expression directed by the Ventral Disc Enhancer in leg discs, suggesting that TnaA acts as a wingless enhancer-specific factor. We describe for the first time the presence of TnaA at the Inner Ring Enhancer as a specific regulator of wingless in the development of wing boundaries.

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“…The GMR driver is expressed in the eye disc and at early pupa stages (Ray and Lakhotia, 2015). To explain why a significant reduction of the target transcript of DHDDS was not detected (C), we refer to Supplementary Figure 2 showing that GMR/GFP is only expressed in the morphogenetic furrow and posterior to it, namely, in a limited volume of the eye disc (Supplementary Figure 2), unlike the situation in the wing disc (Rodríguez et al, 2002). Since we took for the analysis the entire eye-disc, the DHDDS-RNAi was diluted with non-relevant RNA and therefore DHDDS transcript reduction could not be significantly detected.…”

Section: Data Availability Statementmentioning

confidence: 99%

Knockdown of Dehydrodolichyl Diphosphate Synthase in the Drosophila Retina Leads to a Unique Pattern of Retinal Degeneration

Brandwine

Ifrah

Bialistoky

et al. 2021

Front. Mol. Neurosci.

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Dehydrodolichyl diphosphate synthase (DHDDS) is a ubiquitously expressed enzyme that catalyzes cis-prenyl chain elongation to produce the poly-prenyl backbone of dolichol. It appears in all tissues including the nervous system and it is a highly conserved enzyme that can be found in all animal species. Individuals who have biallelic missense mutations in the DHDDS gene are presented with non-syndromic retinitis pigmentosa with unknown underlying mechanism. We have used the Drosophila model to compromise DHDDS ortholog gene (CG10778) in order to look for cellular and molecular mechanisms that, when defective, might be responsible for this retinal disease. The Gal4/UAS system was used to suppress the expression of CG10778 via RNAi-mediated-knockdown in various tissues. The resulting phenotypes were assessed using q-RT-PCR, transmission-electron-microscopy (TEM), electroretinogram, antibody staining and Western blot analysis. Targeted knockdown of CG10778-mRNA in the early embryo using the actin promoter or in the developing wings using the nub promoter resulted in lethality, or wings loss, respectively. Targeted expression of CG10778-RNAi using the glass multiple reporter (GMR)-Gal4 driver (GMR-DHDDS-RNAi) in the larva eye disc and pupal retina resulted in a complex phenotype: (a) TEM retinal sections revealed a unique pattern of retinal-degeneration, where photoreceptors R2 and R5 exhibited a nearly normal structure of their signaling-compartment (rhabdomere), but only at the region of the nucleus, while all other photoreceptors showed retinal degeneration at all regions. (b) Western blot analysis revealed a drastic reduction in rhodopsin levels in GMR-DHDDS-RNAi-flies and TEM sections showed an abnormal accumulation of endoplasmic reticulum (ER). To conclude, compromising DHDDS in the developing retina, while allowing formation of the retina, resulted in a unique pattern of retinal degeneration, characterized by a dramatic reduction in rhodopsin protein level and an abnormal accumulation of ER membranes in the photoreceptors cells, thus indicating that DHDDS is essential for normal retinal formation.

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Different mechanisms initiate and maintainwinglessexpression in theDrosophilawing hinge

Cited by 36 publications

References 51 publications

Shared enhancer gene regulatory networks between wound and oncogenic programs

Shared enhancer gene regulatory networks between wound and oncogenic programs

TnaA, a trithorax group protein, modulates wingless expression in different regions of the Drosophila wing imaginal disc

Knockdown of Dehydrodolichyl Diphosphate Synthase in the Drosophila Retina Leads to a Unique Pattern of Retinal Degeneration

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