Open Access

ARTICLE

Carbon Monoxide Signal Breaks Primary Seed Dormancy by Transcriptional Silence of DOG1 in Arabidopsis thaliana

Danni He, Guoli Deng, Songpei Ying, Wenjuan Yang, Jiali Wei, Ping Li^*

Shanghai Key Laboratory of Bio-Energy Crops, Research Center for Natural Products, Plant Science Center, School of Life Sciences, Shanghai University, Shanghai, 200444, China

* Corresponding Author: Ping Li. Email:

Phyton-International Journal of Experimental Botany 2020, 89(3), 633-643. https://doi.org/10.32604/phyton.2020.010498

Received 07 March 2020; Accepted 10 April 2020; Issue published 22 June 2020

Abstract

Primary seed dormancy is an adaptive strategy that prevents germination for viable seeds in harsh environment, ensuring seeds germination under favorable condition. Accurately inducing seeds germination in a controllable manner is important for crop production. Thus searching the chemicals that efficiently breaks seed dormancy is valuable. DOG1 protein abundance in the freshly harvested seed is high, and its level is correlated to seed dormancy intensity, thus DOG1 is regarded as the timer to evaluate the seed dormancy degree. In this study, we found the carbon monoxide (CO) donor treatment, the transgenic line with high CO content, showed lower seed dormancy, while scavenging CO, or the mutant with lower CO level, presented strong primary seed dormancy, genetic analysis showed that DOG1 was targeted by CO signal and was prerequisite for CO-dependent seed dormancy release. Furthermore, we found CO signal activated the expression of ERF/AP2 transcriptional factor ERF12, as well as enhanced the binding of ERF12 to the promoter of DOG1, ultimately transcriptional silence of DOG1 expression to break primary seed dormancy. Meanwhile CO signal reduced the histone acetylation level at the chromatin of DOG1 locus to suppress its expression. Together, our results revealed that CO acts as the novel regulator to suppress DOG1 expression and efficiently break primary seed dormancy through activating the negative factor ERF12.

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Citations