Jasmonate activates secondary cell wall biosynthesis through MYC2‐MYB46 module

Author:

Im Jong Hee123ORCID,Son Seungmin4ORCID,Kim Won‐Chan5,Kim Kihwan5,Mitsuda Nobutaka6,Ko Jae‐Heung7ORCID,Han Kyung‐Hwan128ORCID

Affiliation:

1. Department of Horticulture Michigan State University East Lansing Michigan 48824 USA

2. DOE Great Lakes Bioenergy Research Center Michigan State University East Lansing Michigan 48824 USA

3. Department of Science Education Jeju National University Jeju Republic of Korea

4. National Institute of Agricultural Sciences Rural Development Administration Jeonju 54874 Republic of Korea

5. School of Applied Biosciences Kyungpook National University Daegu 41566 Republic of Korea

6. Bioproduction Research Institute National Institute of Advanced Industrial Science and Technology Tsukuba 305‐8566 Japan

7. Department of Plant & Environmental New Resources Kyung Hee University Yongin 17104 Republic of Korea

8. Department of Forestry Michigan State University East Lansing Michigan 48824 USA

Abstract

SUMMARYFormation of secondary cell wall (SCW) is tightly regulated spatiotemporally by various developmental and environmental signals. Successful fine‐tuning of the trade‐off between SCW biosynthesis and stress responses requires a better understanding of how plant growth is regulated under environmental stress conditions. However, the current understanding of the interplay between environmental signaling and SCW formation is limited. The lipid‐derived plant hormone jasmonate (JA) and its derivatives are important signaling components involved in various physiological processes including plant growth, development, and abiotic/biotic stress responses. Recent studies suggest that JA is involved in SCW formation but the signaling pathway has not been studied for how JA regulates SCW formation. We tested this hypothesis using the transcription factor MYB46, a master switch for SCW biosynthesis, and JA treatments. Both the transcript and protein levels of MYB46, a master switch for SCW formation, were significantly increased by JA treatment, resulting in the upregulation of SCW biosynthesis. We then show that this JA‐induced upregulation of MYB46 is mediated by MYC2, a central regulator of JA signaling, which binds to the promoter of MYB46. We conclude that this MYC2‐MYB46 module is a key component of the plant response to JA in SCW formation.

Funder

Advanced Low Carbon Technology Research and Development Program

National Research Foundation of Korea

Publisher

Wiley

Subject

Cell Biology,Plant Science,Genetics

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