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Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana

MYB-type transcription factors (TFs) play important roles in plant growth and development, and in the rapid responses to unfavorable environmental conditions. We recently reported the isolation and characterization of a rice (Oryza sativa) MYB TF, OsMYB102, which is involved in the regulation of lea...

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Autores principales: Piao, Weilan, Sakuraba, Yasuhito, Paek, Nam-Chon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society for Biochemistry and Molecular Biology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889895/
https://www.ncbi.nlm.nih.gov/pubmed/31072449
http://dx.doi.org/10.5483/BMBRep.2019.52.11.071
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author Piao, Weilan
Sakuraba, Yasuhito
Paek, Nam-Chon
author_facet Piao, Weilan
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 rapid responses to unfavorable environmental conditions. We recently reported the isolation and characterization of a rice (Oryza sativa) MYB TF, OsMYB102, which is involved in the regulation of leaf senescence by downregulating abscisic acid (ABA) biosynthesis and the downstream signaling response. Based on the similarities of their sequences and expression patterns, OsMYB102 appears to be a homolog of the Arabidopsis thaliana AtMYB44 TF. Since AtMYB44 is a key regulator of leaf senescence and abiotic stress responses, it is important to examine whether AtMYB44 homologs in other plants also act similarly. Here, we generated transgenic Arabidopsis plants expressing OsMYB102 (OsMYB102-OX). The OsMYB102-OX plants showed a delayed senescence phenotype during dark incubation and were more susceptible to salt and drought stresses, considerably similar to Arabidopsis plants overexpressing AtMYB44. Real-time quantitative PCR (RT-qPCR) revealed that, in addition to known senescence-associated genes, genes encoding the ABA catabolic enzymes AtCYP707A3 and AtCYP707A4 were also significantly upregulated in OsMYB102-OX, leading to a significant decrease in ABA accumulation. Furthermore, protoplast transient expression and chromatin immunoprecipitation assays revealed that OsMYB102 directly activated AtCYP707A3 expression. Based on our findings, it is probable that the regulatory functions of AtMYB44 homologs in plants are highly conserved and they have vital roles in leaf senescence and the abiotic stress responses.
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spelling pubmed-68898952019-12-10 Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana Piao, Weilan Sakuraba, Yasuhito Paek, Nam-Chon BMB Rep Articles MYB-type transcription factors (TFs) play important roles in plant growth and development, and in the rapid responses to unfavorable environmental conditions. We recently reported the isolation and characterization of a rice (Oryza sativa) MYB TF, OsMYB102, which is involved in the regulation of leaf senescence by downregulating abscisic acid (ABA) biosynthesis and the downstream signaling response. Based on the similarities of their sequences and expression patterns, OsMYB102 appears to be a homolog of the Arabidopsis thaliana AtMYB44 TF. Since AtMYB44 is a key regulator of leaf senescence and abiotic stress responses, it is important to examine whether AtMYB44 homologs in other plants also act similarly. Here, we generated transgenic Arabidopsis plants expressing OsMYB102 (OsMYB102-OX). The OsMYB102-OX plants showed a delayed senescence phenotype during dark incubation and were more susceptible to salt and drought stresses, considerably similar to Arabidopsis plants overexpressing AtMYB44. Real-time quantitative PCR (RT-qPCR) revealed that, in addition to known senescence-associated genes, genes encoding the ABA catabolic enzymes AtCYP707A3 and AtCYP707A4 were also significantly upregulated in OsMYB102-OX, leading to a significant decrease in ABA accumulation. Furthermore, protoplast transient expression and chromatin immunoprecipitation assays revealed that OsMYB102 directly activated AtCYP707A3 expression. Based on our findings, it is probable that the regulatory functions of AtMYB44 homologs in plants are highly conserved and they have vital roles in leaf senescence and the abiotic stress responses. Korean Society for Biochemistry and Molecular Biology 2019-11 2019-11-30 /pmc/articles/PMC6889895/ /pubmed/31072449 http://dx.doi.org/10.5483/BMBRep.2019.52.11.071 Text en Copyright © 2019 by the The Korean Society for Biochemistry and Molecular Biology 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 unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Piao, Weilan
Sakuraba, Yasuhito
Paek, Nam-Chon
Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title_full Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title_fullStr Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title_full_unstemmed Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title_short Transgenic expression of rice MYB102 (OsMYB102) delays leaf senescence and decreases abiotic stress tolerance in Arabidopsis thaliana
title_sort transgenic expression of rice myb102 (osmyb102) delays leaf senescence and decreases abiotic stress tolerance in arabidopsis thaliana
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889895/
https://www.ncbi.nlm.nih.gov/pubmed/31072449
http://dx.doi.org/10.5483/BMBRep.2019.52.11.071
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