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盐胁迫应答中细胞分裂素缺乏的转录组分析揭示了细胞分裂素缺乏的差异调节作用。

Transcriptome analyses of a salt-tolerant cytokinin-deficient mutant reveal differential regulation of salt stress response by cytokinin deficiency.

机构信息

Signaling Pathway Research Unit, RIKEN Plant Science Center, Yokohama, Kanagawa, Japan.

出版信息

PLoS One. 2012;7(2):e32124. doi: 10.1371/journal.pone.0032124. Epub 2012 Feb 15.

DOI:10.1371/journal.pone.0032124
PMID:22355415
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3280229/
Abstract

Soil destruction by abiotic environmental conditions, such as high salinity, has resulted in dramatic losses of arable land, giving rise to the need of studying mechanisms of plant adaptation to salt stress aimed at creating salt-tolerant plants. Recently, it has been reported that cytokinins (CKs) regulate plant environmental stress responses through two-component systems. A decrease in endogenous CK levels could enhance salt and drought stress tolerance. Here, we have investigated the global transcriptional change caused by a reduction in endogenous CK content under both normal and salt stress conditions. Ten-day-old Arabidopsis thaliana wild-type (WT) and CK-deficient ipt1,3,5,7 plants were transferred to agar plates containing either 0 mM (control) or 200 mM NaCl and maintained at normal growth conditions for 24 h. Our experimental design allowed us to compare transcriptome changes under four conditions: WT-200 mM vs. WT-0 mM, ipt1,3,5,7-0 mM vs. WT-0 mM, ipt1,3,5,7-200 mM vs. ipt1,3,5,7-0 mM and ipt1,3,5,7-200 mM vs. WT-200 mM NaCl. Our results indicated that the expression of more than 10% of all of the annotated Arabidopsis genes was altered by CK deficiency under either normal or salt stress conditions when compared to WT. We found that upregulated expression of many genes encoding either regulatory proteins, such as NAC, DREB and ZFHD transcription factors and the calcium sensor SOS3, or functional proteins, such as late embryogenesis-abundant proteins, xyloglucan endo-transglycosylases, glycosyltransferases, glycoside hydrolases, defensins and glyoxalase I family proteins, may contribute to improved salt tolerance of CK-deficient plants. We also demonstrated that the downregulation of photosynthesis-related genes and the upregulation of several NAC genes may cause the altered morphological phenotype of CK-deficient plants. This study highlights the impact of CK regulation on the well-known stress-responsive signaling pathways, which regulate plant adaptation to high salinity as well as other environmental stresses.

摘要

非生物环境条件(如高盐度)导致土壤破坏,导致可耕地大量丧失,因此需要研究植物适应盐胁迫的机制,旨在创造耐盐植物。最近,据报道细胞分裂素(CKs)通过双组分系统调节植物环境胁迫反应。内源性 CK 水平的降低可增强植物对盐和干旱胁迫的耐受性。在这里,我们研究了在正常和盐胁迫条件下降低内源性 CK 含量引起的全局转录变化。将 10 天大的拟南芥野生型(WT)和 CK 缺陷型 ipt1,3,5,7 植物转移到含有 0 mM(对照)或 200 mM NaCl 的琼脂平板上,并在正常生长条件下维持 24 h。我们的实验设计允许我们在四种条件下比较转录组变化:WT-200 mM 与 WT-0 mM、ipt1,3,5,7-0 mM 与 WT-0 mM、ipt1,3,5,7-200 mM 与 ipt1,3,5,7-0 mM 和 ipt1,3,5,7-200 mM 与 WT-200 mM NaCl。结果表明,与 WT 相比,在正常或盐胁迫条件下,CK 缺乏会改变超过 10%的所有已注释的拟南芥基因的表达。我们发现,许多编码调节蛋白(如 NAC、DREB 和 ZFHD 转录因子以及钙传感器 SOS3)或功能蛋白(如晚期胚胎丰富蛋白、木葡聚糖内切糖基转移酶、糖基转移酶、糖苷水解酶、防御素和乙醛酸酶 I 家族蛋白)的基因表达上调可能有助于提高 CK 缺陷植物的耐盐性。我们还证明,光合作用相关基因的下调和几个 NAC 基因的上调可能导致 CK 缺陷植物改变的形态表型。这项研究强调了 CK 调节对众所周知的应激反应信号通路的影响,这些信号通路调节植物对高盐度以及其他环境胁迫的适应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/d9227bc3b592/pone.0032124.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/cdf0962906ab/pone.0032124.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/de60efdf13d0/pone.0032124.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/d0d44b044d74/pone.0032124.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/8dd999fe8d26/pone.0032124.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/73218e7c3890/pone.0032124.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/d9227bc3b592/pone.0032124.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/cdf0962906ab/pone.0032124.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/de60efdf13d0/pone.0032124.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/d0d44b044d74/pone.0032124.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/8dd999fe8d26/pone.0032124.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/73218e7c3890/pone.0032124.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/304d/3280229/d9227bc3b592/pone.0032124.g006.jpg

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