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Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1 a group III histidine kinase

机译:烟草中链格孢菌侵袭的转录组学分析揭示了由AlHK1(III组组氨酸激酶)调节的发病机理

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摘要

Tobacco brown spot, caused by Alternaria species, is a devastating tobacco disease. To explore the role of a group III histidine kinase (AlHK1) on A. longipes pathogenesis, the invasion progress of A. longipes was monitored. We found that the wild-type strain C-00 invaded faster than the AlHK1-disrupted strain HK∆4 in the early and middle infection stages and the reverse trend occurred in the late infection stage. Then, eight invasion transcriptomes were performed using RNA-Seq and 205 shared, 505 C-00 and 222 HK∆4 specific differentially expressed genes (DEGs) were identified. The annotation results showed seven antioxidant activity genes were specifically identified in the HKΔ4 DEGs. A subsequent experiment confirmed that HKΔ4 was more resistant to low concentrations oxidative stress than C-00. In addition, the results from 1) statistics for the number of DEGs, GO enriched terms, DEGs in clusters with rising trends, and 2) analyses of the expression patterns of some DEGs relevant for osmoadaptation and virulence showed that changes in C-00 infection existed mainly in the early and middle stages, while HKΔ4 infection arose mainly in the late stage. Our results reveal firstly the pathogenesis of A. longipes regulated by AlHK1 and provide useful insights into the fungal-plant interactions.
机译:烟草链球菌引起的烟草褐斑是毁灭性的烟草病。为了探索III组组氨酸激酶(AlHK1)在长曲霉发病机理中的作用,监测了长曲霉的入侵进程。我们发现,在感染的早期和中期,野生型菌株C-00的侵袭速度比破坏AlHK1的菌株HK∆4快,而在感染后期则出现了相反的趋势。然后,使用RNA-Seq进行了8个侵袭转录组的转录,共有205个,鉴定出505 C-00和222 HK∆4特异性差异表达基因(DEG)。注释结果显示在HKΔ4DEGs中特异性鉴定了七个抗氧化活性基因。随后的实验证实,HKΔ4比C-00更能抵抗低浓度的氧化应激。此外,以下结果来自:1)统计的DEG数量,GO富集术语,具有上升趋势的簇中的DEG,以及2)对某些与渗透适应性和毒力相关的DEG的表达模式的分析表明C-00感染的变化感染主要发生在早期和中期,而HKΔ4感染主要发生在晚期。我们的研究结果首先揭示了由AlHK1调控的长曲霉的发病机理,并为真菌-植物相互作用提供了有用的见识。

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