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Updated: Jan 28, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
Rice transcription factor OsMYB102 delays leaf senescence by down-regulating abscisic acid accumulation and signaling
Weilan Piao1, Suk-Hwan Kim1, Byoung-Doo Lee1
1Department of Plant Science, Plant Genomics and Breeding Institute, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea.
Abstract:
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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