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Genome-wide RNA-seq analysis indicates that the DAG1 transcription factor promotes hypocotyl elongation acting on ABA, ethylene and auxin signaling

Hypocotyl elongation is influenced by light and hormones, but the molecular mechanisms underlying this process are not yet fully elucidated. We had previously suggested that the Arabidopsis DOF transcription factor DAG1 may be a negative component of the mechanism of light-mediated inhibition of hyp...

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Detalles Bibliográficos
Autores principales: Lorrai, Riccardo, Gandolfi, Francesco, Boccaccini, Alessandra, Ruta, Veronica, Possenti, Marco, Tramontano, Anna, Costantino, Paolo, Lepore, Rosalba, Vittorioso, Paola
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6203721/
https://www.ncbi.nlm.nih.gov/pubmed/30367178
http://dx.doi.org/10.1038/s41598-018-34256-3
Descripción
Sumario:Hypocotyl elongation is influenced by light and hormones, but the molecular mechanisms underlying this process are not yet fully elucidated. We had previously suggested that the Arabidopsis DOF transcription factor DAG1 may be a negative component of the mechanism of light-mediated inhibition of hypocotyl elongation, as light-grown dag1 knock-out mutant seedlings show significant shorter hypocotyls than the wild type. By using high-throughput RNA-seq, we compared the transcriptome profile of dag1 and wild type hypocotyls and seedlings. We identified more than 250 genes differentially expressed in dag1 hypocotyls, and their analysis suggests that DAG1 is involved in the promotion of hypocotyl elongation through the control of ABA, ethylene and auxin signaling. Consistently, ChIP-qPCR results show that DAG1 directly binds to the promoters of WRKY18 encoding a transcription factor involved in ABA signaling, of the ethylene- induced gene ETHYLENE RESPONSE FACTOR (ERF2), and of the SMALL AUXIN UP RNA 67 (SAUR67), an auxin-responding gene encoding a protein promoting hypocotyl cell expansion.