ELONGATED HYPOCOTYL 5-mediated suppression of melatonin biosynthesis is alleviated by darkness and promotes cotyledon opening

© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissionsoup.com.

Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany. - 1985. - 73(2022), 14 vom: 11. Aug., Seite 4941-4953
1. Verfasser: Wang, Lin (VerfasserIn)
Weitere Verfasser: Zhou, Fangfang, Liu, Xuan, Zhang, Haixia, Yan, Tianci, Sun, Yanzhao, Shi, Kun, Zheng, Xiaodong, Zhu, Yunpeng, Shan, Dongqian, Bai, Yixue, Guo, Yan, Kong, Jin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2022
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Research Support, Non-U.S. Gov't AtSNAT6 AtCOP1 AtHY5 biosynthesis regulation cotyledon opening melatonin Arabidopsis Proteins Melatonin JL5DK93RCL
Beschreibung
Zusammenfassung:© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissionsoup.com.
Melatonin (N-acetyl-5-methoxytryptamine) biosynthesis in plants is induced by darkness and high-intensity light; however, the underlying transcriptional mechanisms and upstream signalling pathways are unknown. We identified a dark-induced and highly expressed melatonin synthetase in Arabidopsis thaliana, AtSNAT6, encoding serotonin N-acetyltransferase. We assessed melatonin content and AtSNAT6 expression in mutants lacking key regulators of light/dark signalling. AtCOP1 (CONSTITUTIVE PHOTOMORPHOGENIC 1) and AtHY5 (ELONGATED HYPOCOTYL 5), which control light/dark transition and photomorphogenesis, promoted and suppressed melatonin biosynthesis, respectively. Using EMSA and ChIP-qPCR analysis, we showed that AtHY5 inhibits AtSNAT6 expression directly. An analysis of melatonin content in snat6 hy5 double mutant and AtHY5+AtSNAT6-overexpressing plants confirmed the regulatory function of AtHY5 and AtSNAT6 in melatonin biosynthesis. Exogenous melatonin further inhibited cotyledon opening in hy5 mutant and AtSNAT6-overexpressing seedlings, but partially reversed the promotion of cotyledon opening in AtHY5-overexpressing seedlings and snat6. Additionally, CRISPR/Cas9-mediated mutation of AtSNAT6 increased cotyledon opening in hy5 mutant, and overexpression of AtSNAT6 decreased cotyledon opening in AtHY5-overexpressing seedlings via changing melatonin biosynthesis, confirming that AtHY5 decreased melatonin-mediated inhibition of cotyledon opening. Our data provide new insights into the regulation of melatonin biosynthesis and its function in cotyledon opening
Beschreibung:Date Completed 12.08.2022
Date Revised 09.09.2022
published: Print
Citation Status MEDLINE
ISSN:1460-2431
DOI:10.1093/jxb/erac176