J Integr Plant Biol. ›› 2021, Vol. 63 ›› Issue (4): 802-815.DOI: 10.1111/jipb.13062

Special Issue: Hormone signaling

• Plant-abiotic Interactions • Previous Articles    

Mediator tail module subunits MED16 and MED25 differentially regulate abscisic acid signaling in Arabidopsis

Pengcheng Guo1†, Leelyn Chong1†, Fangming Wu2, Chuan‐Chih Hsu3, Chuanyou Li2, Jian‐Kang Zhu4,5 and Yingfang Zhu1*   

  1. 1State Key Laboratory of Crop Stress Adaptation and Improvement, Key Laboratory of Cotton Biology, School of Life Sciences, Henan University, Kaifeng 475001, China
    2State Key Laboratory of Plant Genomics, National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Innovation Academy for Seed Design, the Chinese Academy of Sciences, Beijing 100101, China
    3Institute of Plant and Microbial Biology, Academia Sinica, Taipei 11529
    4Shanghai Center for Plant Stress Biology, Shanghai Institutes for Biological Sciences, the Chinese Academy of Sciences, Shanghai 200032, China
    5Department of Horticulture and Landscape Architecture, Purdue University, West LafayetteIndiana 47907, USA

    These authors contributed equally to this work.
    *Correspondence: Yingfang Zhu (zhuyf@henu.edu.cn)
  • Received:2020-09-07 Accepted:2020-12-19 Online:2020-12-23 Published:2021-04-01

Abstract: MED25 has been implicated as a negative regulator of the abscisic acid (ABA) signaling pathway. However, it is unclear whether other Mediator subunits could associate with MED25 to participate in the ABA response. Here, we used affinity purification followed by mass spectrometry to uncover Mediator subunits that associate with MED25 in transgenic plants. We found that at least 26 Mediator subunits, belonging to the head, middle, tail, and CDK8 kinase modules, were co‐purified with MED25 in vivo. Interestingly, the tail module subunit MED16 was identified to associate with MED25 under both mock and ABA treatments. We further showed that the disruption of MED16 led to reduced ABA sensitivity compared to the wild type. Transcriptomic analysis revealed that the expression of several ABA‐responsive genes was significantly lower in med16 than those in wild type. Furthermore, we discovered that MED16 may possibly compete with MED25 to interact with the key transcription factor ABA INSENSITIVE 5 (ABI5) to positively regulate ABA signaling. Consistently, med16 and med25 mutants displayed opposite phenotypes in ABA response, cuticle permeability, and differential ABI5‐mediated EM1 and EM6 expression. Together, our data indicate that MED16 and MED25 differentially regulate ABA signaling by antagonistically affecting ABI5‐mediated transcription in Arabidopsis.

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