Transcriptome Analysis of the Molecular Patterns of Pear Plants Infected by Two Colletotrichum fructicola Pathogenic Strains Causing Contrasting Sets of Leaf Symptoms.
Transcriptome Analysis of the Molecular Patterns of Pear Plants Infected by Two Colletotrichum fructicola Pathogenic Strains Causing Contrasting Sets of Leaf Symptoms.
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两种梨炭疽病原菌株感染引起对比鲜明的叶子症状的梨植物的分子模式的转录组分析
DOI：
10.3389/fpls.2022.761133
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发表时间：
2022
影响因子：
5.6
通讯作者：
Wang G
中科院分区：
文献类型：
--
作者：
Fu M;Bai Q;Zhang H;Guo Y;Peng Y;Zhang P;Shen L;Hong N;Xu W;Wang G
果炭疽菌感染梨叶，导致两种主要症状：微小黑斑（TS），随后严重的早期落叶和大坏死病灶（BnL），根据致病型，没有明显损害。相同的真菌种类如何引起不同的症状仍不清楚。为了了解由此引起的疾病和不同症状的分子机制，将两种 C. fructicola 致病菌株（分别导致 TS 和 BnL 症状的 PAFQ31 和 PAFQ32）接种在梨叶梨叶上，并分别在静止期 (QS) 和坏死营养期 (NS) 进行转录组测序。在植物中，各菌株感染导致 NS 处参与水杨酸 (SA) 信号通路的基因上调。相比之下，乙烯（ET）、脱落酸（ABA）和茉莉酸（JA）信号通路与菌株PAFQ31感染引起的TS症状特异性相关，对应于菌株感染引发的黄化和早期落叶症状。相应地，使用高效液相色谱法测量，在 NS 时各菌株感染的叶片中 SA 积累水平相似，但在 PAFQ31 感染的叶片中 JA 明显较高。加权基因共表达网络分析还揭示了与 PAFQ31 相关的早期落叶相关的特定基因、途径、植物激素和转录因子 (TF)。总而言之，这些数据表明，P. perifolia 中的特定代谢途径受到调节，以响应两种 C. fructicola 致病型的感染，从而导致不同的症状：JA、ET 和 ABA 在 PAFQ31 感染的叶子中积累，这对叶绿素代谢和光合作用途径产生负面影响，同时对衰老相关 TF 和基因的表达产生积极影响，导致叶子变黄和落叶；而SA抑制了PAFQ32感染叶片中JA诱导的基因表达，从而导致过敏反应样反应和BnL症状。
Colletotrichum fructicola infects pear leaves, resulting in two major symptoms: tiny black spots (TS) followed by severe early defoliation and big necrotic lesions (BnL) without apparent damage depending on the pathotypes. How the same fungal species causes different symptoms remains unclear. To understand the molecular mechanism underlying the resulting diseases and the diverse symptoms, two C. fructicola pathogenetic strains (PAFQ31 and PAFQ32 responsible for TS and BnL symptoms, respectively) were inoculated on Pyrus pyrifolia leaves and subjected to transcriptome sequencing at the quiescent stage (QS) and necrotrophic stage (NS), respectively. In planta, the genes involved in the salicylic acid (SA) signaling pathway were upregulated at the NS caused by the infection of each strain. In contrast, the ethylene (ET), abscisic acid (ABA), and jasmonic acid (JA) signaling pathways were specifically related to the TS symptoms caused by the infection of strain PAFQ31, corresponding to the yellowish and early defoliation symptoms triggered by the strain infection. Correspondingly, SA was accumulated in similar levels in the leaves infected by each strain at NS, but JA was significantly higher in the PAFQ31-infected as measured using high-performance liquid chromatography. Weighted gene co-expression network analysis also reveals specific genes, pathways, phytohormones, and transcription factors (TFs) associated with the PAFQ31-associated early defoliation. Taken together, these data suggest that specific metabolic pathways were regulated in P. pyrifolia in response to the infection of two C. fructicola pathotypes resulting in the diverse symptoms: JA, ET, and ABA accumulated in the PAFQ31-infected leaves, which negatively affected the chlorophyll metabolism and photosynthesis pathways while positively affecting the expression of senescence-associated TFs and genes, resulted in leaf yellowing and defoliation; whereas SA inhibited JA-induced gene expression in the PAFQ32-infected leaves, which led to hypersensitive response-like reaction and BnL symptoms.
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作者：
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