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茉莉酸和细胞分裂素在木质部发育中的拮抗作用。

Antagonistic interaction between jasmonic acid and cytokinin in xylem development.

机构信息

Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, 151-921, Korea.

Graduate School of International Agricultural Technology and Crop Biotechnology Institute/Green BioScience and Technology, Seoul National University, Pyeongchang, 232-916, Korea.

出版信息

Sci Rep. 2017 Aug 31;7(1):10212. doi: 10.1038/s41598-017-10634-1.

Abstract

Developmental flexibility under stress conditions largely relies on the interactions between hormones that mediate stress responses and developmental processes. In this study, we showed that the stress hormone jasmonic acid (JA) induces formation of extra xylem in the roots of wild-type Arabidopsis thaliana (Col-0). JA signaling mutants such as coronatine insensitive1-1 and jasmonate resistant1-1 did not form extra xylem in response to JA, but the JA biosynthesis mutant oxophytodienoate-reductase3 did form extra xylem. These observations suggested that the JA response promotes xylem development. To understand the mechanism, we examined the regulatory interaction between JA and cytokinin, a negative regulator of xylem development. JA treatment reduced cytokinin responses in the vasculature, and exogenous cytokinin nullified the effect of JA on formation of extra xylem. A time-course experiment showed that suppression of cytokinin responses by JA does not occur rapidly, but the JA-mediated xylem phenotype is tightly linked to the suppression of the cytokinin response. Further analysis of arabidopsis histidine phosphotransfer protein6-1 and myc2-3 mutants revealed that the JA-responsive transcription factor MYC2 regulates the expression of AHP6 in response to JA and expression of AHP6 is involved in the JA-mediated xylem phenotype.

摘要

在应激条件下,发育的灵活性在很大程度上依赖于介导应激反应和发育过程的激素之间的相互作用。在这项研究中,我们表明应激激素茉莉酸(JA)诱导野生型拟南芥(Col-0)根中额外木质部的形成。JA 信号突变体,如冠菌素不敏感 1-1 和茉莉酸抗性 1-1,对 JA 没有形成额外木质部,但 JA 生物合成突变体 oxophytodienoate-reductase3 确实形成了额外木质部。这些观察结果表明,JA 反应促进了木质部的发育。为了理解这一机制,我们研究了 JA 和细胞分裂素之间的调节相互作用,细胞分裂素是木质部发育的负调节剂。JA 处理降低了脉管系统中细胞分裂素的反应,而外源细胞分裂素则消除了 JA 对额外木质部形成的影响。时程实验表明,JA 对细胞分裂素反应的抑制作用不是迅速发生的,而是 JA 介导的木质部表型与细胞分裂素反应的抑制密切相关。对拟南芥组氨酸磷酸转移蛋白 6-1 和 myc2-3 突变体的进一步分析表明,JA 反应转录因子 MYC2 调节 AHP6 的表达以响应 JA,并且 AHP6 的表达参与了 JA 介导的木质部表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af59/5579306/a0c6df6dca48/41598_2017_10634_Fig1_HTML.jpg

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