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纳米孔测序与混合组装:通过增强注释和耐药性分析揭示美元斑病的基因组图谱

Nanopore sequencing and hybrid assembly: unraveling the genomic landscape of dollar spot with enhanced annotation and drug resistance profiling.

作者信息

Shi Xiaojing, Zhao Shu, Gibbons John G, Jung Geunhwa

机构信息

Stockbridge School of Agriculture, University of Massachusetts, Amherst, MA, United States.

Department of Food Science, University of Massachusetts, Amherst, MA, United States.

出版信息

Front Fungal Biol. 2025 Jul 17;6:1621663. doi: 10.3389/ffunb.2025.1621663. eCollection 2025.

DOI:10.3389/ffunb.2025.1621663
PMID:40747239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12310695/
Abstract

The increasing multi-drug resistance observed in the turfgrass pathogen spp. has emerged as a critical issue. Understanding the mechanisms underlying fungicide resistance is crucial to address this challenge. This study focuses on comparing a highly propiconazole-resistant isolate of , HRI11, with a sensitive isolate, HRS10. Genomes were sequenced using the Oxford Nanopore MinION sequencing platform, and hybrid assembly was performed using this data and existing Pacific Biosciences long reads and Illumina short reads. HRI11 genome assembly represents the most contiguous and complete genome assembly reported for to date, spanning 43.6 MB with 12,831 predicted protein-coding genes across 51 scaffolds. In contrast, the HRS10 had an assembly size of 39.6 MB and encoded 12,161 putative proteins distributed over 100 scaffolds. While the two isolates share substantial sequence similarity and overall protein content, the fungicide resistance observed in HRI11 appears to arise primarily from genetic variants, particularly in genes encoding transcription factors, transporters, and fungicide target genes. These genetic variants establish a foundational resistance level against fungicides. Furthermore, induced resistance in HRI11 involves increased expression of proteins that facilitate fungicide efflux, thereby optimizing energy allocation during fungicide exposures. Together, these mechanisms-inherent genetic variation and adaptive transcriptional responses-contribute to the heightened resilience of HRI11 under fungicide treatment.

摘要

在草坪草病原菌中观察到的多药耐药性不断增加,已成为一个关键问题。了解杀菌剂抗性的潜在机制对于应对这一挑战至关重要。本研究重点比较了对丙环唑高度耐药的菌株HRI11和敏感菌株HRS10。使用牛津纳米孔MinION测序平台对基因组进行测序,并利用这些数据以及现有的太平洋生物科学公司的长读长和Illumina短读长进行混合组装。HRI11基因组组装代表了迄今为止报道的最连续和完整的基因组组装,跨越43.6MB,在51个支架上有12831个预测的蛋白质编码基因。相比之下,HRS10的组装大小为39.6MB,编码12161个推定蛋白质,分布在100个支架上。虽然这两个菌株具有大量的序列相似性和总体蛋白质含量,但HRI11中观察到的杀菌剂抗性似乎主要源于遗传变异,特别是在编码转录因子、转运蛋白和杀菌剂靶基因的基因中。这些遗传变异建立了对杀菌剂的基本抗性水平。此外,HRI11中的诱导抗性涉及促进杀菌剂外排的蛋白质表达增加,从而在杀菌剂暴露期间优化能量分配。总之,这些机制——固有的遗传变异和适应性转录反应——有助于提高HRI11在杀菌剂处理下的恢复力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/ebddb4e20f07/ffunb-06-1621663-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/bc25e18e10d2/ffunb-06-1621663-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/5fd7db29cb7a/ffunb-06-1621663-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/110dd9f1f466/ffunb-06-1621663-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/e2e2253e2ba1/ffunb-06-1621663-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/ebddb4e20f07/ffunb-06-1621663-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/bc25e18e10d2/ffunb-06-1621663-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/0138af282c36/ffunb-06-1621663-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/110dd9f1f466/ffunb-06-1621663-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/e2e2253e2ba1/ffunb-06-1621663-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a92/12310695/ebddb4e20f07/ffunb-06-1621663-g008.jpg

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