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丛枝菌根共生导致番茄叶片中与细胞壁相关的基因和微小RNA的差异调控。

Arbuscular Mycorrhizal Symbiosis Leads to Differential Regulation of Genes and miRNAs Associated with the Cell Wall in Tomato Leaves.

作者信息

Mendoza-Soto Ana Belén, Rodríguez-Corral Amada Zulé, Bojórquez-López Adriana, Cervantes-Rojo Maylin, Castro-Martínez Claudia, Lopez-Meyer Melina

机构信息

Departamento Biotecnología Agrícola, Instituto Politécnico Nacional, CIIDIR-Sinaloa, Blv. Juan de Dios Bátiz 250, Guasave 81000, Mexico.

出版信息

Biology (Basel). 2022 Jun 2;11(6):854. doi: 10.3390/biology11060854.

DOI:10.3390/biology11060854
PMID:35741375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9219611/
Abstract

Arbuscular mycorrhizal symbiosis is an association that provides nutritional benefits to plants. Importantly, it induces a physiological state allowing plants to respond to a subsequent pathogen attack in a more rapid and intense manner. Consequently, mycorrhiza-colonized plants become less susceptible to root and shoot pathogens. This study aimed to identify some of the molecular players and potential mechanisms related to the onset of defense priming by mycorrhiza colonization, as well as miRNAs that may act as regulators of priming genes. The upregulation of cellulose synthases, pectinesterase inhibitors, and xyloglucan endotransglucosylase/hydrolase, as well as the downregulation of a pectinesterase, suggest that the modification and reinforcement of the cell wall may prime the leaves of mycorrhizal plants to react faster and stronger to subsequent pathogen attack. This was confirmed by the findings of miR164a-3p, miR164a-5p, miR171e-5p, and miR397, which target genes and are also related to the biosynthesis or modification of cell wall components. Our findings support the hypothesis that the reinforcement or remodeling of the cell wall and cuticle could participate in the priming mechanism triggered by mycorrhiza colonization, by strengthening the first physical barriers upstream of the pathogen encounter.

摘要

丛枝菌根共生是一种为植物提供营养益处的共生关系。重要的是,它会诱导一种生理状态,使植物能够以更快、更强烈的方式应对随后的病原体攻击。因此,被菌根定殖的植物对根和茎病原体的易感性降低。本研究旨在确定一些与菌根定殖引发防御预激活相关的分子参与者和潜在机制,以及可能作为预激活基因调节因子的miRNA。纤维素合酶、果胶酯酶抑制剂和木葡聚糖内转糖基酶/水解酶的上调,以及一种果胶酯酶的下调,表明细胞壁的修饰和强化可能使菌根植物的叶片对随后的病原体攻击做出更快、更强的反应。靶向基因且也与细胞壁成分的生物合成或修饰相关的miR164a - 3p、miR164a - 5p、miR171e - 5p和miR397的研究结果证实了这一点。我们的研究结果支持这样一种假设,即细胞壁和角质层的强化或重塑可能通过加强病原体接触上游的第一道物理屏障,参与菌根定殖引发的预激活机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/0039267a9456/biology-11-00854-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/1a339d6706d5/biology-11-00854-g0A1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/66e6c66a9c28/biology-11-00854-g0A2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/4722b9894f1f/biology-11-00854-g0A3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/541aab7271fc/biology-11-00854-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/b3c235408ad7/biology-11-00854-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/d3e1c6170c4d/biology-11-00854-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/b33518d04817/biology-11-00854-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/7e899a5b47bf/biology-11-00854-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/0039267a9456/biology-11-00854-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/1a339d6706d5/biology-11-00854-g0A1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/66e6c66a9c28/biology-11-00854-g0A2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/4722b9894f1f/biology-11-00854-g0A3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/541aab7271fc/biology-11-00854-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/b3c235408ad7/biology-11-00854-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/d3e1c6170c4d/biology-11-00854-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/b33518d04817/biology-11-00854-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/7e899a5b47bf/biology-11-00854-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f55d/9219611/0039267a9456/biology-11-00854-g006.jpg

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