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LSD1 控制的水杨酸积累对于非生物胁迫引发细胞死亡至关重要。

Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress.

机构信息

Institute of Technology and Life Sciences, Falenty, Al. Hrabska 3, 05-090 Raszyn, Poland.

Department of Botany, Institute of Biology, Warsaw University of Life Sciences, Nowoursynowska Street 159, 02-776 Warsaw, Poland.

出版信息

Cells. 2021 Apr 20;10(4):962. doi: 10.3390/cells10040962.

DOI:10.3390/cells10040962
PMID:33924244
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8074770/
Abstract

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in . The mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the with the mutant, caring mutation in ) gene and having deregulated SA synthesis, and with plants expressing the bacterial gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the mutant exhibited clear cell death phenotype, which was reversed in and / plants. The expression of -genes and the HO content in UV-treated were significantly higher when compared with the wild type. In contrast, and / plants demonstrated comparability with the wild-type level of -genes expression and HO. Our results demonstrate that SA accumulation is crucial for triggering cell death in , while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

摘要

水杨酸(SA)是一种众所周知的参与细胞死亡调控的激素分子。植物对广泛的环境因素(如高光、UV、病原体攻击)做出反应时会积累 SA,SA 参与诱导和扩散某些叶片细胞的死亡。LESION SIMULATING DISEASE 1(LSD1)是 中最著名的细胞死亡调节剂之一。突变体缺乏功能性 LSD1 蛋白,会积累 SA,并且对许多生物和非生物胁迫条件具有易感性。为了更深入地了解 LSD1 依赖的 SA 积累在细胞死亡过程中的调节作用,我们将 突变体与 突变体(在 基因中带有突变,导致 SA 合成失调)和表达细菌 基因的植物(能够将 SA 分解为儿茶酚)进行杂交。在 UV A+B 照射下,突变体表现出明显的细胞死亡表型,而在 和 /植物中则得到了逆转。与野生型相比,UV 处理的 中 -基因的表达和 HO 含量显著升高。相比之下,和 /植物的 -基因表达和 HO 水平与野生型相当。我们的结果表明,SA 积累对于触发 中的细胞死亡至关重要,而减少过量的 SA 积累可能会导致对非生物胁迫的耐受性更强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/e545c25f8527/cells-10-00962-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/6dcb209455f8/cells-10-00962-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/01564c973111/cells-10-00962-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/de1a229248f1/cells-10-00962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/e545c25f8527/cells-10-00962-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/6dcb209455f8/cells-10-00962-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/01564c973111/cells-10-00962-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/de1a229248f1/cells-10-00962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1fd/8074770/e545c25f8527/cells-10-00962-g004.jpg

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