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叶绿体氧化还原状态变化标志着细胞间信号在超敏反应中的传递。

Chloroplast redox state changes mark cell-to-cell signaling in the hypersensitive response.

机构信息

National Institute of Biology, Večna pot 111, 1000, Ljubljana, Slovenia.

Laboratory of Genetics, University of Wisconsin - Madison, Madison, WI, 53706, USA.

出版信息

New Phytol. 2023 Jan;237(2):548-562. doi: 10.1111/nph.18425. Epub 2022 Sep 1.

DOI:10.1111/nph.18425
PMID:35946378
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9875368/
Abstract

Hypersensitive response (HR)-conferred resistance is associated with induction of programmed cell death and pathogen spread restriction in its proximity. The exact role of chloroplastic reactive oxygen species and its link with salicylic acid (SA) signaling in HR remain unexplained. To unravel this, we performed a detailed spatiotemporal analysis of chloroplast redox response in palisade mesophyll and upper epidermis to potato virus Y (PVY) infection in a resistant potato genotype and its transgenic counterpart with impaired SA accumulation and compromised resistance. Besides the cells close to the cell death zone, we detected individual cells with oxidized chloroplasts further from the cell death zone. These are rare in SA-deficient plants, suggesting their role in signaling for resistance. We confirmed that chloroplast redox changes play important roles in signaling for resistance, as blocking chloroplast redox changes affected spatial responses at the transcriptional level. Through spatiotemporal study of stromule induction after PVY infection, we show that stromules are induced by cell death and also as a response to PVY multiplication at the front of infection. Overall induction of stromules is attenuated in SA-deficient plants.

摘要

超敏反应 (HR) 赋予的抗性与诱导程序性细胞死亡和限制其邻近病原体扩散有关。质体活性氧及其与水杨酸 (SA) 信号转导的联系在 HR 中的确切作用仍未得到解释。为了解开这个谜团,我们对马铃薯 Y 病毒 (PVY) 在抗性马铃薯基因型及其转基因对应物中的质体氧化还原反应进行了详细的时空分析,这些对应物的 SA 积累受损,抗性受损。除了靠近细胞死亡区的细胞外,我们还在远离细胞死亡区的单个细胞中检测到氧化的质体。在 SA 缺陷型植物中,这些细胞很少见,表明它们在抗性信号转导中发挥作用。我们证实,质体氧化还原变化在抗性信号转导中起着重要作用,因为阻断质体氧化还原变化会影响转录水平上的空间反应。通过对 PVY 感染后 stromule 诱导的时空研究,我们表明 stromule 是由细胞死亡诱导的,也是对感染前沿处 PVY 增殖的反应。SA 缺陷型植物中 stromule 的整体诱导减弱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/0c47dca90610/NPH-237-548-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/0c47dca90610/NPH-237-548-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/d3ebf6deca16/NPH-237-548-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/a43fd2a16c88/NPH-237-548-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/aab72233bfef/NPH-237-548-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a8d/10087015/0c47dca90610/NPH-237-548-g001.jpg

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