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乙烯合成基因和乙烯受体基因在调控[植物名称]开花时间、花药开裂和花朵衰老过程中影响赤霉素-DELLA和茉莉酸信号传导。

The Ethylene Synthesis Gene and Ethylene Receptor Gene Affect GA-DELLA and Jasmonic Acid Signaling in Regulating Flowering Time, Anther Dehiscence, and Flower Senescence in .

作者信息

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

机构信息

Institute of Biotechnology, National Chung Hsing University, Taichung, Taiwan.

Advanced Plant Biotechnology Center, National Chung Hsing University, Taichung, Taiwan.

出版信息

Front Plant Sci. 2022 Apr 1;13:785441. doi: 10.3389/fpls.2022.785441. eCollection 2022.

Abstract

In plants, the key enzyme in ethylene biosynthesis is 1-aminocyclopropane-1 carboxylic acid (ACC) synthase (ACS), which catalyzes -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 and in orchids, () and () from Gower Ramsey were functionally analyzed in . 35S:: caused late flowering and anther indehiscence phenotypes due to its effect on GA-DELLA signaling pathways. 35S:: repressed GA biosynthesis genes (, , and ), which caused the upregulation of DELLA [ (), (), and ] expression. The increase in DELLAs not only suppressed () expression and caused late flowering but also repressed the jasmonic acid (JA) biosynthesis gene and caused anther indehiscence by downregulating the endothecium-thickening-related genes , , and . The ectopic expression of an dominant-negative mutation () caused both ethylene and JA insensitivity in . 35S:: delayed flower/leaf senescence by suppressing downstream genes in ethylene signaling, including and , and in JA signaling, including and . JA signaling repression also resulted in indehiscent anthers the downregulation of , , , and . These results not only provide new insight into the functions of and orthologs but also uncover their functional interactions with other hormone signaling pathways, such as GA-DELLA and JA, in plants.

摘要

在植物中,乙烯生物合成的关键酶是1-氨基环丙烷-1-羧酸(ACC)合酶(ACS),它催化S-腺苷-L-甲硫氨酸(SAM)生成ACC,ACC是乙烯的前体。乙烯与其受体结合,如乙烯反应1(ETR1),以开启乙烯信号转导。为了了解蝴蝶兰中PhACS1和PhACS2的功能,对来自大花蕙兰的PhACS1(PhACS1)和PhACS2(PhACS2)进行了功能分析。35S::PhACS1由于其对GA-DELLA信号通路的影响,导致开花延迟和花药不开裂表型。35S::PhACS1抑制了GA生物合成基因(GA20ox1、GA20ox2和GA3ox1),这导致DELLA[RGA(RGA)、GAI(GAI)和RGL1(RGL1)]表达上调。DELLA的增加不仅抑制了PhFT(PhFT)表达并导致开花延迟,还抑制了茉莉酸(JA)生物合成基因LOX2,并通过下调与内皮增厚相关的基因MYB26、MYB61和TDR,导致花药不开裂。一个显性负突变体(etr1-1)的异位表达导致蝴蝶兰对乙烯和JA均不敏感。35S::PhACS2通过抑制乙烯信号下游基因,包括EIN3和EIL1,以及JA信号下游基因,包括JAZ1和JAZ5,延迟了花/叶衰老。JA信号抑制还导致花药不开裂,这是由于MYB26、MYB61、TDR和EAT1的下调所致。这些结果不仅为PhACS1和PhACS2直系同源基因的功能提供了新的见解,还揭示了它们在植物中与其他激素信号通路,如GA-DELLA和JA的功能相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3036/9011138/22029dcbc956/fpls-13-785441-g001.jpg

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