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由结瘤外蛋白P2介导的a与ORS3257之间共生不亲和机制的阐释。

Elucidation of the symbiotic incompatibility mechanisms between a and ORS3257 mediated by nodulation outer protein P2.

作者信息

Songwattana Pongpan, Boonchuen Pakpoom, Pruksametanan Natcha, Teamtisong Kamonluck, Sato Shusei, Hashimoto Shun, Higashitani Nahoko, Kawaharada Yasuyuki, Araragi Masato, Okazaki Shin, Piromyou Pongdet, Wongdee Jenjira, Greetatorn Teerana, Giraud Eric, Boonkerd Nantakorn, Tittabutr Panlada, Teaumroong Neung

机构信息

Institute of Research and Development, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand.

School of Biotechnology, Institute of Agricultural Technology, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand.

出版信息

iScience. 2025 Apr 4;28(5):112351. doi: 10.1016/j.isci.2025.112351. eCollection 2025 May 16.

DOI:10.1016/j.isci.2025.112351
PMID:40384928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12083990/
Abstract

ORS3257 is an efficient symbiotic strain for and but fails with due to an effector-triggered immunity response mediated by the nodulation outer protein P2 (NopP2). To understand this incompatibility, we identified NopP2 interacting proteins in cv. KPS1, including enolase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), monodehydroascorbate reductase (MDHAR), and serine hydroxymethyltransferase (SHMT) as targets. Protein-protein interaction assays confirmed that NopP2 binds to these enzymes, and further analysis revealed their co-localization on the plasma membrane. Comparative transcriptomic analysis revealed NopP2 stimulates genes related to plant defense response (, , , and ), hydrogen peroxide (, , and ), and cell wall lignification (). NopP2 did not alter the expression of genes encoding the target enzymes but interfered with MDHAR activity, leading to high HO accumulation in roots. These findings suggest that NopP2 contributes to symbiotic incompatibility in by inducing a multifaceted defense response and initiating cell wall lignification early in infection.

摘要

ORS3257是针对[具体植物1]和[具体植物2]的高效共生菌株，但由于结瘤外蛋白P2（NopP2）介导的效应物触发免疫反应，在[具体植物3]上失败。为了解这种不兼容性，我们在[植物品种]cv. KPS1中鉴定了与NopP2相互作用的蛋白质，包括烯醇化酶、甘油醛-3-磷酸脱氢酶（GAPDH）、单脱氢抗坏血酸还原酶（MDHAR）和丝氨酸羟甲基转移酶（SHMT）作为靶点。蛋白质-蛋白质相互作用分析证实NopP2与这些酶结合，进一步分析揭示它们在质膜上共定位。比较转录组分析表明，NopP2刺激与植物防御反应（[相关基因1]、[相关基因2]、[相关基因3]和[相关基因4]）、过氧化氢（[相关基因5]、[相关基因6]和[相关基因7]）以及细胞壁木质化（[相关基因8]）相关的基因。NopP2没有改变编码靶酶的基因表达，但干扰了MDHAR活性，导致根部高浓度的HO积累。这些发现表明，NopP2通过诱导多方面的防御反应并在感染早期启动细胞壁木质化，导致[植物品种]的共生不兼容性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/d742b57ec80d/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/f6f4d9b6e997/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/932577f90ffd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/fa2a477f13e9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/ef7ded61bb5c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/6d6c2a5628a0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/93184c091134/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/87a4da9b6d16/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/1121f2fc5025/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/de0b2a477d1c/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/6a00ce9c0790/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/d742b57ec80d/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/f6f4d9b6e997/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/932577f90ffd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/fa2a477f13e9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/ef7ded61bb5c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/6d6c2a5628a0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/93184c091134/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/87a4da9b6d16/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/1121f2fc5025/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/de0b2a477d1c/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/6a00ce9c0790/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc3/12083990/d742b57ec80d/gr10.jpg

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G-type receptor-like kinase AsNIP43 interacts with rhizobia effector nodulation outer protein P and is required for symbiosis.G 型受体样激酶 AsNIP43 与根瘤菌效应因子 nodulation outer protein P 相互作用，是共生所必需的。
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