Gene expression following induction of regeneration in Drosophila wing imaginal discs. Expression profile of regenerating wing discs

Blanco, Enrique; Ruiz-Romero, Marina; Beltrán, Sergi; Bosch, Manel; Punset, Adrià; Serras, Florenci; Corominas, Montserrat

doi:10.1186/1471-213x-10-94

Cited by 60 publications

(79 citation statements)

References 78 publications

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“…This accurate sampling procedure made it possible to produce highly pure samples and a detailed comparison of gene expression changes in the early regenerating process. Several previous studies published transcriptome data from regenerating discs (17,19,33,34). However, comparing clusters I and III with these datasets, we found that rather few genes were shared with these studies.…”

Section: Upd Activates Jak/stat Signaling In Early Regenerating Discs Tomentioning

confidence: 67%

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During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

Katsuyama

Comoglio

Seimiya

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

117

150

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Regeneration of fragmented Drosophila imaginal discs occurs in an epimorphic manner involving local cell proliferation at the wound site. After disc fragmentation, cells at the wound site activate a restoration program through wound healing, regenerative cell proliferation, and repatterning of the tissue. However, the interplay of signaling cascades driving these early reprogramming steps is not well-understood. Here, we profiled the transcriptome of regenerating cells in the early phase within 24 h after wounding. We found that JAK/STAT signaling becomes activated at the wound site and promotes regenerative cell proliferation in cooperation with Wingless (Wg) signaling. In addition, we showed that the expression of Drosophila insulin-like peptide 8 (dilp8), which encodes a paracrine peptide to delay the onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs. Our findings suggest that JAK/STAT signaling plays a pivotal role in coordinating regenerative disc growth with organismal developmental timing.

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Section: Upd Activates Jak/stat Signaling In Early Regenerating Discs Tomentioning

confidence: 67%

“…Blanco et al (19) analyzed the transcriptome of regenerating wing discs at 24 and 72 h after fragmentation. The results of Blanco et al (19) uncovered the involvement of Notch signaling, cabut and absent, small or homeotic discs 2 in wound healing and regenerative cell proliferation.…”

mentioning

confidence: 97%

During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

Katsuyama

Comoglio

Seimiya

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

117

150

View full text Add to dashboard Cite

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“…S3A). Using these reference controls and mRNA from whole wing imaginal discs, we detected elevated relative expression of genes that are upregulated after tissue damage, such as puckered and cabut (Blanco et al, 2010), or expressed only outside the ablation zone, such as teashirt (Wu and Cohen, 2002;Fig. S3B-D).…”

Section: Analysis Of the Role Of Trithorax During Regenerationmentioning

confidence: 99%

Trithorax regulates systemic signaling duringDrosophilaimaginal disc regeneration

2015

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Although tissue regeneration has been studied in a variety of organisms, from Hydra to humans, many of the genes that regulate the ability of each animal to regenerate remain unknown. The larval imaginal discs of the genetically tractable model organism Drosophila melanogaster have complex patterning, wellcharacterized development and a high regenerative capacity, and are thus an excellent model system for studying mechanisms that regulate regeneration. To identify genes that are important for wound healing and tissue repair, we have carried out a genetic screen for mutations that impair regeneration in the wing imaginal disc. Through this screen we identified the chromatin-modification gene trithorax as a key regeneration gene. Here we show that animals heterozygous for trithorax are unable to maintain activation of a developmental checkpoint that allows regeneration to occur. This defect is likely to be caused by abnormally high expression of puckered, a negative regulator of Jun N-terminal kinase (JNK) signaling, at the wound site. Insufficient JNK signaling leads to insufficient expression of an insulin-like peptide, dILP8, which is required for the developmental checkpoint. Thus, trithorax regulates regeneration signaling and capacity.

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“…Two-color microarray design and analyses were carried out as previously reported (Beltran et al, 2007;Blanco et al, 2010). Total RNA was extracted from eyeantenna imaginal discs from wandering blue-gut staged early third instar larvae using the RNeasy Protect Mini Kit (Qiagen Inc., Valencia, CA, USA).…”

Section: Microarray Analysesmentioning

confidence: 99%

β amyloid protein precursor-like (Appl) is a Ras1/MAPK-regulated gene required for axonal targeting in Drosophila photoreceptor neurons

Mora

Almudí

Alsina

et al. 2013

Journal of Cell Science

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SummaryIn a genome-wide expression profile search for genes required for Drosophila R7 photoreceptor development we found b amyloid protein precursor-like (Appl), the ortholog of human APP, which is a key factor in the pathogenesis of Alzheimer's disease. We analyzed Appl expression in the eye imaginal disc and found that is highly accumulated in R7 photoreceptor cells. The R7 photoreceptor is responsible for UV light detection. To explore the link between high expression of Appl and R7 function, we have analyzed Appl null mutants and found reduced preference for UV light, probably because of mistargeted R7 axons. Moreover, axon mistargeting and inappropriate light discrimination are enhanced in combination with neurotactin mutants. R7 differentiation is triggered by the inductive interaction between R8 and R7 precursors, which results in a burst of Ras1/MAPK, activated by the tyrosine kinase receptor Sevenless. Therefore, we examined whether Ras1/MAPK is responsible for the high Appl expression. Inhibition of Ras1 signaling leads to reduced Appl expression, whereas constitutive activation drives ectopic Appl expression. We show that Appl is directly regulated by the Ras/ MAPK pathway through a mechanism mediated by PntP2, an ETS transcription factor that specifically binds ETS sites in the Appl regulatory region. We also found that zebrafish appb expression increased after ectopic fgfr activation in the neural tube of zebrafish embryos, suggesting a conserved regulatory mechanism.

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Gene expression following induction of regeneration in Drosophila wing imaginal discs. Expression profile of regenerating wing discs

Cited by 60 publications

References 78 publications

During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

Trithorax regulates systemic signaling duringDrosophilaimaginal disc regeneration

β amyloid protein precursor-like (Appl) is a Ras1/MAPK-regulated gene required for axonal targeting in Drosophila photoreceptor neurons

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