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COMPASS组分Ccl1的缺失降低了H3K4三甲基化水平,并影响两种植物病原物种中次生代谢物基因的转录。

Lack of the COMPASS Component Ccl1 Reduces H3K4 Trimethylation Levels and Affects Transcription of Secondary Metabolite Genes in Two Plant-Pathogenic Species.

作者信息

Studt Lena, Janevska Slavica, Arndt Birgit, Boedi Stefan, Sulyok Michael, Humpf Hans-Ulrich, Tudzynski Bettina, Strauss Joseph

机构信息

Division of Microbial Genetics and Pathogen Interactions, Department of Applied Genetics and Cell Biology, BOKU-University of Natural Resources and Life SciencesVienna, Tulln an der Donau, Austria; Institute for Plant Biology and Biotechnology, Westfälische Wilhelms UniversityMünster, Germany.

Institute for Plant Biology and Biotechnology, Westfälische Wilhelms University Münster, Germany.

出版信息

Front Microbiol. 2017 Jan 9;7:2144. doi: 10.3389/fmicb.2016.02144. eCollection 2016.

DOI:10.3389/fmicb.2016.02144
PMID:28119673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5220078/
Abstract

In the two fungal pathogens and , secondary metabolites (SMs) are fitness and virulence factors and there is compelling evidence that the coordination of SM gene expression is under epigenetic control. Here, we characterized Ccl1, a subunit of the COMPASS complex responsible for methylating lysine 4 of histone H3 (H3K4me). We show that Ccl1 is not essential for viability but a regulator of genome-wide trimethylation of H3K4 (H3K4me3). Although, recent work in and spp. detected only sporadic H3K4 methylation at the majority of the SM gene clusters, we show here that SM profiles in deletion mutants are strongly deviating from the wild type. Cross-complementation experiments indicate high functional conservation of Ccl1 as phenotypes of the respective △ were rescued in both fungi. Strikingly, biosynthesis of the species-specific virulence factors gibberellic acid and deoxynivalenol produced by and , respectively, was reduced in axenic cultures but virulence was not attenuated in these mutants, a phenotype which goes in line with restored virulence factor production levels This suggests that yet unknown plant-derived signals are able to compensate for Ccl1 function during pathogenesis.

摘要

在两种真菌病原体和中,次生代谢产物(SMs)是适应性和毒力因子,并且有确凿证据表明SM基因表达的协调受表观遗传控制。在此,我们对Ccl1进行了表征,它是负责组蛋白H3赖氨酸4(H3K4me)甲基化的COMPASS复合物的一个亚基。我们表明Ccl1对生存力不是必需的,但它是全基因组H3K4三甲基化(H3K4me3)的调节因子。尽管最近在和属物种中的研究在大多数SM基因簇中仅检测到零星的H3K4甲基化,但我们在此表明缺失突变体中的SM谱与野生型有很大差异。交叉互补实验表明Ccl1具有高度的功能保守性,因为在两种真菌中各自△的表型都得到了挽救。令人惊讶的是,和分别产生的物种特异性毒力因子赤霉素和脱氧雪腐镰刀菌烯醇的生物合成在无菌培养中减少,但这些突变体的毒力并未减弱,这一表型与毒力因子产生水平的恢复一致。这表明在发病过程中,尚不清楚的植物衍生信号能够补偿Ccl1的功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/b3c1f4710535/fmicb-07-02144-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/2ca28e5618e9/fmicb-07-02144-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/db44be612fed/fmicb-07-02144-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/4dd071c86685/fmicb-07-02144-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/2a631c3455f0/fmicb-07-02144-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/41464b4e9c9e/fmicb-07-02144-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/b3c1f4710535/fmicb-07-02144-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/2ca28e5618e9/fmicb-07-02144-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/db44be612fed/fmicb-07-02144-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/4dd071c86685/fmicb-07-02144-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/2a631c3455f0/fmicb-07-02144-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/41464b4e9c9e/fmicb-07-02144-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0780/5220078/b3c1f4710535/fmicb-07-02144-g006.jpg

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