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WGCNA 揭示了大豆对 感染反应的枢纽基因和关键基因调控途径。

WGCNA Reveals Hub Genes and Key Gene Regulatory Pathways of the Response of Soybean to Infection by .

机构信息

College of Life Sciences, Shanxi Agricultural University, Taigu, Jinzhong 030801, China.

College of Agronomy, Shanxi Agricultural University, Taigu, Jinzhong 030801, China.

出版信息

Genes (Basel). 2024 Apr 27;15(5):566. doi: 10.3390/genes15050566.

DOI:10.3390/genes15050566
PMID:38790195
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11120672/
Abstract

(SMV) is one of the main pathogens that can negatively affect soybean production and quality. To study the gene regulatory network of soybeans in response to SMV SC15, the resistant line X149 and susceptible line X97 were subjected to transcriptome analysis at 0, 2, 8, 12, 24, and 48 h post-inoculation (hpi). Differential expression analysis revealed that 10,190 differentially expressed genes (DEGs) responded to SC15 infection. Weighted gene co-expression network analysis (WGCNA) was performed to identify highly related resistance gene modules; in total, eight modules, including 2256 DEGs, were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of 2256 DEGs revealed that the genes significantly clustered into resistance-related pathways, such as the plant-pathogen interaction pathway, mitogen-activated protein kinases (MAPK) signaling pathway, and plant hormone signal transduction pathway. Among these pathways, we found that the flg22, Ca, hydrogen peroxide (HO), and abscisic acid (ABA) regulatory pathways were fully covered by 36 DEGs. Among the 36 DEGs, the gene (protein phosphatase 2C, PP2C) in the ABA regulatory pathway, the gene (WRKY transcription factor 22, WRKY22) in Ca and HO regulatory pathways, and the gene (calcium-dependent protein kinase, CDPK) in Ca regulatory pathways were highly connected hub genes. These results indicate that the resistance of X149 to SC15 may depend on the positive regulation of flg22, Ca, HO, and ABA regulatory pathways. Our study further showed that superoxide dismutase (SOD) activity, HO content, and catalase (CAT) and peroxidase (POD) activities were significantly up-regulated in the resistant line X149 compared with those in 0 hpi. This finding indicates that the HO regulatory pathway might be dependent on flg22- and Ca-pathway-induced ROS generation. In addition, two hub genes, encoding F-box protein) and (encoding calmodulin-like proteins, CMLs), were also identified and they could positively regulate X149 resistance. This study provides pathways for further investigation of SMV resistance mechanisms in soybean.

摘要

(SMV)是一种主要的病原体,它会对大豆的生产和质量产生负面影响。为了研究大豆对 SMV SC15 的基因调控网络,采用 X149 抗性系和 X97 感病系进行了接种后 0、2、8、12、24 和 48 小时的转录组分析。差异表达分析显示,10190 个差异表达基因(DEGs)对 SC15 感染有反应。采用加权基因共表达网络分析(WGCNA)鉴定了高度相关的抗性基因模块;共鉴定到 8 个模块,包含 2256 个 DEGs。对 2256 个 DEGs 的京都基因与基因组百科全书(KEGG)通路富集分析显示,这些基因显著聚类到与抗性相关的通路,如植物-病原体互作通路、丝裂原活化蛋白激酶(MAPK)信号通路和植物激素信号转导通路。在这些通路中,我们发现 flg22、Ca、过氧化氢(HO)和脱落酸(ABA)调节通路完全由 36 个 DEGs 覆盖。在 36 个 DEGs 中,ABA 调节通路中的基因 (蛋白磷酸酶 2C,PP2C)、Ca 和 HO 调节通路中的基因 (WRKY 转录因子 22,WRKY22)和 Ca 调节通路中的基因 (钙依赖型蛋白激酶,CDPK)是高度连接的枢纽基因。这些结果表明,X149 对 SC15 的抗性可能依赖于 flg22、Ca、HO 和 ABA 调节通路的正调控。我们的研究进一步表明,与 0 hpi 相比,抗性系 X149 中的超氧化物歧化酶(SOD)活性、HO 含量以及过氧化氢酶(CAT)和过氧化物酶(POD)活性显著上调。这一发现表明,HO 调节通路可能依赖于 flg22 和 Ca 通路诱导的 ROS 产生。此外,还鉴定到两个枢纽基因,分别编码 F-box 蛋白和钙调素样蛋白(CMLs),它们可以正向调控 X149 的抗性。本研究为进一步研究大豆对 SMV 的抗性机制提供了途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/92246954d3cd/genes-15-00566-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/07086a9f276a/genes-15-00566-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/af86935af2bb/genes-15-00566-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/f6346e8226a1/genes-15-00566-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/69bf40203335/genes-15-00566-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/b352aabeae44/genes-15-00566-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/31e7626ab5af/genes-15-00566-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/289bee03d6c6/genes-15-00566-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/75c473f9409f/genes-15-00566-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/92246954d3cd/genes-15-00566-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/07086a9f276a/genes-15-00566-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/af86935af2bb/genes-15-00566-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/f6346e8226a1/genes-15-00566-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/69bf40203335/genes-15-00566-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/b352aabeae44/genes-15-00566-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/31e7626ab5af/genes-15-00566-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/289bee03d6c6/genes-15-00566-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/75c473f9409f/genes-15-00566-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede7/11120672/92246954d3cd/genes-15-00566-g009.jpg

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