Regulation of PYR/PYL/RCAR ABA receptors mRNA stability: involvement of miR5628 in decay of PYL6 mRNA
Vieira, J. G. P.; Duarte, G. T.; Barrera-Rojas, C. H.; Matiolli, C. C.; Viana, A. J. C.; Canesin, L. E. D.; Vicentini, R.; Nogueira, F. T.; Vincentz, M. G. A.
Show abstract
Hormone signaling fine-tuning involves feedback regulatory loops. Abscisic acid (ABA) plays key functions in development and tolerance to abiotic stress. ABA is sensed by the PYR/PYL/RCAR receptors and it also represses their gene expression. Conversely, ABA induces PP2C phosphatases expression, which are negative regulators of the ABA signaling pathway. This feedback regulatory scheme is likely important for the modulation of ABA signal transduction. Here, we provide a new insight into the mechanisms underlying the ABA-induced negative control of PYR/PYL/RCAR expression in Arabidopsis thaliana. The strong and sustained repression of PYR/PYL/RCARs revealed by ABA time course treatment defines the regulation of receptors genes as an important step in resetting the ABA signaling pathway. Transcription inhibition by cordycepin showed that destabilization of PYL1/4/5/6 mRNA is involved in ABA-induced repression of these genes. Furthermore, genetic evidence indicated that decapping may play a role in PYL4/5/6 mRNAs decay. In addition, we provide evidence that the Arabidopsis-specific microRNA5628 (miR5628), which is transiently induced by the ABA core signaling pathway, guides the cleavage of PYL6 transcript in response to ABA. After cleavage, the resulting RISC 5- and 3-cleaved fragments of PYL6 mRNA may be degraded by exoribonuclease XRN4. MiR5628 is an evolutionary novelty that may contribute, with decapping and XRN4 activities, to enhance PYL6 mRNA degradation. Thus, control of stability of PYR/PYL/RCAR transcripts is an important step in maintaining homeostasis of ABA signaling. One Sentence SummaryAttenuation of ABA signaling involves destabilization of PYL1/4/5/6 transcripts. ABA core signaling induces miR5628 expression to enhance PYL6 mRNA degradation in conjunction with decapping and XRN4 activities.
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