AUTHOR=Feng Yaqiong , Yin Zhiyuan , Wu Yuxing , Xu Liangsheng , Du Hongxia , Wang Nana , Huang Lili 

TITLE=LaeA Controls Virulence and Secondary Metabolism in Apple Canker Pathogen Valsa mali

JOURNAL=Frontiers in Microbiology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2020.581203

DOI=10.3389/fmicb.2020.581203

ISSN=1664-302X

ABSTRACT=<p>Apple Valsa canker is a destructive disease caused by the ascomycete <italic>Valsa mali</italic> and poses a serious threat to apple production. Toxins synthesized by secondary metabolite biosynthetic gene clusters (SMBGCs) have been proven to be crucial for pathogen virulence. A previous study showed that <italic>V. mali</italic> genome contains remarkably expanded SMBGCs and some of their genes were significantly upregulated during infection. In this study, we focus on LaeA, a known regulator of secondary metabolism, for its role in SMBGC regulation, toxin production, and virulence of <italic>V. mali</italic>. Deletion of <italic>VmLaeA</italic> led to greatly reduced virulence with lesion length reduced by 48% on apple twigs. Toxicity tests proved that toxicity of secondary metabolites (SMs) produced by <italic>VmLaeA</italic> deletion mutant (Δ<italic>VmlaeA</italic>) was markedly decreased in comparison with wild-type (WT). Transcriptomic and proteomic analyses of WT and Δ<italic>VmlaeA</italic> indicated that a portion of transporters and about half (31/60) SMBGCs are regulated by <italic>VmLaeA.</italic> Function analysis of eight gene clusters including <italic>PKS7</italic>, <italic>PKS11</italic>, <italic>NRPS14</italic>, <italic>PKS16</italic>, <italic>PKS23</italic>, <italic>PKS31</italic>, <italic>NRPS/PKS33</italic>, and <italic>PKS39</italic> that were differentially expressed at both transcriptional and translational levels showed that four of them (i.e., <italic>PKS11</italic>, <italic>PKS16</italic>, <italic>PKS23</italic>, and <italic>PKS31</italic>) were involved in pigment production and <italic>NRPS14</italic> contributed to virulence. Our findings will provide new insights and gene resources for understanding the role of pathogenicity-related toxins in <italic>V. mali</italic>.</p>