AUTHOR=Huang Tzu-Hsiang , Hsu Wei-Han , Mao Wan-Ting , Yang Chang-Hsien 

TITLE=The Oncidium Ethylene Synthesis Gene Oncidium 1-Aminocyclopropane-1 Carboxylic Acid Synthase 12 and Ethylene Receptor Gene Oncidium ETR1 Affect GA–DELLA and Jasmonic Acid Signaling in Regulating Flowering Time, Anther Dehiscence, and Flower Senescence in Arabidopsis

JOURNAL=Frontiers in Plant Science

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2022.785441

DOI=10.3389/fpls.2022.785441

ISSN=1664-462X

ABSTRACT=<p>In plants, the key enzyme in ethylene biosynthesis is 1-aminocyclopropane-1 carboxylic acid (ACC) synthase (ACS), which catalyzes <italic>S</italic>-adenosyl-L-methionine (SAM) to ACC, the precursor of ethylene. Ethylene binds to its receptors, such as ethylene response 1 (ETR1), to switch on ethylene signal transduction. To understand the function of <italic>ACS</italic> and <italic>ETR1</italic> in orchids, <italic>Oncidium ACC synthase 12</italic> (<italic>OnACS12</italic>) and <italic>Oncidium ETR1</italic> (<italic>OnETR1</italic>) from <italic>Oncidium</italic> Gower Ramsey were functionally analyzed in <italic>Arabidopsis</italic>. 35S::<italic>OnACS12</italic> caused late flowering and anther indehiscence phenotypes due to its effect on GA–DELLA signaling pathways. 35S::<italic>OnACS12</italic> repressed GA biosynthesis genes (<italic>CPS</italic>, <italic>KS</italic>, and <italic>GA3ox1</italic>), which caused the upregulation of DELLA [<italic>GA-INSENSITIVE</italic> (<italic>GAI</italic>), <italic>RGA-LIKE1</italic> (<italic>RGL1</italic>), and <italic>RGL2</italic>] expression. The increase in DELLAs not only suppressed <italic>LEAFY</italic> (<italic>LFY</italic>) expression and caused late flowering but also repressed the jasmonic acid (JA) biosynthesis gene <italic>DAD1</italic> and caused anther indehiscence by downregulating the endothecium-thickening-related genes <italic>MYB26</italic>, <italic>NST1</italic>, and <italic>NST2</italic>. The ectopic expression of an <italic>OnETR1</italic> dominant-negative mutation (<italic>OnETR1-C65Y</italic>) caused both ethylene and JA insensitivity in <italic>Arabidopsis</italic>. 35S::<italic>OnETR1-C65Y</italic> delayed flower/leaf senescence by suppressing downstream genes in ethylene signaling, including <italic>EDF1-4</italic> and <italic>ERF1</italic>, and in JA signaling, including <italic>MYC2</italic> and <italic>WRKY33</italic>. JA signaling repression also resulted in indehiscent anthers <italic>via</italic> the downregulation of <italic>MYB26</italic>, <italic>NST1</italic>, <italic>NST2</italic>, and <italic>MYB85</italic>. These results not only provide new insight into the functions of <italic>ACS</italic> and <italic>ETR1</italic> orthologs but also uncover their functional interactions with other hormone signaling pathways, such as GA–DELLA and JA, in plants.</p>