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Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling

MYB-type transcription factors (TFs) play important roles in plant growth and development, and in the responses to several abiotic stresses. In rice (Oryza sativa), the roles of MYB-related TFs in leaf senescence are not well documented. Here, we examined rice MYB TF gene OsMYB102 and found that an...

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Autores principales: Piao, Weilan, Kim, Suk-Hwan, Lee, Byoung-Doo, An, Gynheung, Sakuraba, Yasuhito, Paek, Nam-Chon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6506775/
https://www.ncbi.nlm.nih.gov/pubmed/30825376
http://dx.doi.org/10.1093/jxb/erz095
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author Piao, Weilan
Kim, Suk-Hwan
Lee, Byoung-Doo
An, Gynheung
Sakuraba, Yasuhito
Paek, Nam-Chon
author_facet Piao, Weilan
Kim, Suk-Hwan
Lee, Byoung-Doo
An, Gynheung
Sakuraba, Yasuhito
Paek, Nam-Chon
author_sort Piao, Weilan
collection PubMed
description MYB-type transcription factors (TFs) play important roles in plant growth and development, and in the responses to several abiotic stresses. In rice (Oryza sativa), the roles of MYB-related TFs in leaf senescence are not well documented. Here, we examined rice MYB TF gene OsMYB102 and found that an OsMYB102 T-DNA activation-tagged line (termed osmyb102-D), which constitutively expresses OsMYB102 under the control of four tandem repeats of the 35S promoter, and OsMYB102-overexpressing transgenic lines (35S:OsMYB102 and 35S:GFP-OsMYB102) maintain green leaves much longer than the wild-type under natural, dark-induced, and abscisic acid (ABA)-induced senescence conditions. Moreover, an osmyb102 knockout mutant showed an accelerated senescence phenotype under dark-induced and ABA-induced leaf senescence conditions. Microarray analysis showed that a variety of senescence-associated genes (SAGs) were down-regulated in the osmyb102-D line. Further studies demonstrated that overexpression of OsMYB102 controls the expression of SAGs, including genes associated with ABA degradation and ABA signaling (OsABF4, OsNAP, and OsCYP707A6), under dark-induced senescence conditions. OsMYB102 inhibits ABA accumulation by directly activating the transcription of OsCYP707A6, which encodes the ABA catabolic enzyme ABSCISIC ACID 8′-HYDROXYLASE. OsMYB102 also indirectly represses ABA-responsive genes, such as OsABF4 and OsNAP. Collectively, these results demonstrate that OsMYB102 plays a critical role in leaf senescence by down-regulating ABA accumulation and ABA signaling responses.
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spelling pubmed-65067752019-05-13 Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling Piao, Weilan Kim, Suk-Hwan Lee, Byoung-Doo An, Gynheung Sakuraba, Yasuhito Paek, Nam-Chon J Exp Bot Research Papers MYB-type transcription factors (TFs) play important roles in plant growth and development, and in the responses to several abiotic stresses. In rice (Oryza sativa), the roles of MYB-related TFs in leaf senescence are not well documented. Here, we examined rice MYB TF gene OsMYB102 and found that an OsMYB102 T-DNA activation-tagged line (termed osmyb102-D), which constitutively expresses OsMYB102 under the control of four tandem repeats of the 35S promoter, and OsMYB102-overexpressing transgenic lines (35S:OsMYB102 and 35S:GFP-OsMYB102) maintain green leaves much longer than the wild-type under natural, dark-induced, and abscisic acid (ABA)-induced senescence conditions. Moreover, an osmyb102 knockout mutant showed an accelerated senescence phenotype under dark-induced and ABA-induced leaf senescence conditions. Microarray analysis showed that a variety of senescence-associated genes (SAGs) were down-regulated in the osmyb102-D line. Further studies demonstrated that overexpression of OsMYB102 controls the expression of SAGs, including genes associated with ABA degradation and ABA signaling (OsABF4, OsNAP, and OsCYP707A6), under dark-induced senescence conditions. OsMYB102 inhibits ABA accumulation by directly activating the transcription of OsCYP707A6, which encodes the ABA catabolic enzyme ABSCISIC ACID 8′-HYDROXYLASE. OsMYB102 also indirectly represses ABA-responsive genes, such as OsABF4 and OsNAP. Collectively, these results demonstrate that OsMYB102 plays a critical role in leaf senescence by down-regulating ABA accumulation and ABA signaling responses. Oxford University Press 2019-05-01 2019-03-02 /pmc/articles/PMC6506775/ /pubmed/30825376 http://dx.doi.org/10.1093/jxb/erz095 Text en © Society for Experimental Biology 2019. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Research Papers
Piao, Weilan
Kim, Suk-Hwan
Lee, Byoung-Doo
An, Gynheung
Sakuraba, Yasuhito
Paek, Nam-Chon
Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title_full Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title_fullStr Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title_full_unstemmed Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title_short Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
title_sort rice transcription factor osmyb102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6506775/
https://www.ncbi.nlm.nih.gov/pubmed/30825376
http://dx.doi.org/10.1093/jxb/erz095
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