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dc.contributor.author
Da Ros, Vanina Gabriela
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dc.contributor.author
Gutierrez-Perez, Irene
dc.contributor.author
Ferres-Marco, Dolors
dc.contributor.author
Dominguez, María
dc.date.available
2015-05-15T18:31:11Z
dc.date.issued
2013-05-07
dc.identifier.citation
Da Ros, Vanina Gabriela; Gutierrez-Perez, Irene; Ferres-Marco, Dolors; Dominguez, María; Dampening the signals transduced through hedgehog via microRNA miR-7 facilitates Notch-induced tumourigenesis; Public Library Science; Plos Biology; 11; 2013-5; 1001554-1001554;
dc.identifier.issn
1544-9173
dc.identifier.uri
http://hdl.handle.net/11336/489
dc.description.abstract
Fine-tuned Notch and Hedgehog signaling pathways via attenuators and dampers have long been recognized as important<br />mechanisms to ensure the proper size and differentiation of many organs and tissues. This notion is further supported by<br />identification of mutations in these pathways in human cancer cells. However, although it is common that the Notch and<br />Hedgehog pathways influence growth and patterning within the same organ through the establishment of organizing<br />regions, the cross-talk between these two pathways and how the distinct organizing activities are integrated during growth<br />is poorly understood. Here, in an unbiased genetic screen in the Drosophila melanogaster eye, we found that tumour-like<br />growth was provoked by cooperation between the microRNA miR-7 and the Notch pathway. Surprisingly, the molecular<br />basis of this cooperation between miR-7 and Notch converged on the silencing of Hedgehog signalling. In mechanistic<br />terms, miR-7 silenced the interference hedgehog (ihog) Hedgehog receptor, while Notch repressed expression of the brother<br />of ihog (boi) Hedgehog receptor. Tumourigenesis was induced co-operatively following Notch activation and reduced<br />Hedgehog signalling, either via overexpression of the microRNA or through specific down-regulation of ihog, hedgehog,<br />smoothened, or cubitus interruptus or via overexpression of the cubitus interruptus repressor form. Conversely, increasing<br />Hedgehog signalling prevented eye overgrowth induced by the microRNA and Notch pathway. Further, we show that<br />blocking Hh signal transduction in clones of cells mutant for smoothened also enhance the organizing activity and growth<br />by Delta-Notch signalling in the wing primordium. Together, these findings uncover a hitherto unsuspected tumour<br />suppressor role for the Hedgehog signalling and reveal an unanticipated cooperative antagonism between two pathways<br />extensively used in growth control and cancer.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Public Library Science
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Drosophila
dc.subject
Microrna
dc.subject
Notch
dc.subject
Hedgehog
dc.subject.classification
Ciencias Naturales y Exactas
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
Biología del Desarrollo
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dc.title
Dampening the signals transduced through hedgehog via microRNA miR-7 facilitates Notch-induced tumourigenesis
dc.type
info:eu-repo/semantics/article
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dc.type
info:eu-repo/semantics/publishedVersion
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dc.type
info:ar-repo/semantics/artículo
dc.date.updated
2016-03-30 10:35:44.97925-03
dc.journal.volume
11
dc.journal.number
5
dc.journal.pagination
1001554-1001554
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
San Francisco
dc.description.fil
Fil: Da Ros,Vanina Gabriela . CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS. INST.DE NEUROCIENCIA DE ALICANTE.
dc.description.fil
Fil: Gutierrez-Perez, Irene. CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS. INST.DE NEUROCIENCIA DE ALICANTE.
dc.description.fil
Fil: Ferres-Marco, Dolors. CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS. INST.DE NEUROCIENCIA DE ALICANTE.
dc.description.fil
Fil: Dominguez M. CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS. INST.DE NEUROCIENCIA DE ALICANTE.
dc.journal.title
Plos Biology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/doi:10.1371/journal.pbio.1001554
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