Yu Jisuk, Kim Kook-Hyung
Plant Genomics and Breeding Institute, Seoul National University, Seoul, South Korea.
Department of Agricultural Biotechnology, College of Agriculture and Life Sciences, Seoul, South Korea.
Front Microbiol. 2021 Feb 11;12:622261. doi: 10.3389/fmicb.2021.622261. eCollection 2021.
The Fusarium graminearum virus 1 (FgV1) causes noticeable phenotypic changes such as reduced mycelial growth, increase pigmentation, and reduced pathogenicity in its host fungi, . Previous study showed that the numerous genes including regulatory factors were differentially expressed upon FgV1 infection, however, we have limited knowledge on the effect(s) of specific transcription factor (TF) during FgV1 infection in host fungus. Using gene-deletion mutant library of 657 putative TFs in , we transferred FgV1 by hyphal anastomosis to screen transcription factors that might be associated with viral replication or symptom induction. FgV1-infected TF deletion mutants were divided into three groups according to the mycelial growth phenotype compare to the FgV1-infected wild-type strain (WT-VI). The FgV1-infected TF deletion mutants in Group 1 exhibited slow or weak mycelial growth compare to that of WT-VI on complete medium at 5 dpi. In contrast, Group 3 consists of virus-infected TF deletion mutants showing faster mycelial growth and mild symptom compared to that of WT-VI. The hyphal growth of FgV1-infected TF deletion mutants in Group 2 was not significantly different from that of WT-VI. We speculated that differences of mycelial growth among the FgV1-infected TF deletion mutant groups might be related with the level of FgV1 RNA accumulations in infected host fungi. By conducting real-time quantitative reverse transcription polymerase chain reaction, we observed close association between FgV1 RNA accumulation and phenotypic differences of FgV1-infected TF deletion mutants in each group, i.e., increased and decreased dsRNA accumulation in Group 1 and Group 3, respectively. Taken together, our analysis provides an opportunity to identify host's regulator(s) of FgV1-triggered signaling and antiviral responses and helps to understand complex regulatory networks between FgV1 and interaction.
禾谷镰刀菌病毒1（FgV1）在其宿主真菌中会引起明显的表型变化，如菌丝生长减缓、色素沉着增加和致病性降低。先前的研究表明，包括调控因子在内的众多基因在FgV1感染后差异表达，然而，我们对宿主真菌在FgV1感染期间特定转录因子（TF）的作用了解有限。利用[具体物种]中657个假定转录因子的基因缺失突变体文库，我们通过菌丝吻合转移FgV1，以筛选可能与病毒复制或症状诱导相关的转录因子。与FgV1感染的野生型菌株（WT-VI）相比，根据菌丝生长表型，将FgV1感染的转录因子缺失突变体分为三组。在5 dpi时，第1组中FgV1感染的转录因子缺失突变体在完全培养基上的菌丝生长比WT-VI缓慢或微弱。相反，第3组由病毒感染的转录因子缺失突变体组成，其菌丝生长比WT-VI更快，症状更轻。第2组中FgV1感染的转录因子缺失突变体的菌丝生长与WT-VI没有显著差异。我们推测，FgV1感染的转录因子缺失突变体组之间菌丝生长的差异可能与感染宿主真菌中FgV1 RNA的积累水平有关。通过进行实时定量逆转录聚合酶链反应，我们观察到FgV1 RNA积累与每组中FgV1感染的转录因子缺失突变体的表型差异密切相关，即第1组和第3组中双链RNA积累分别增加和减少。综上所述，我们的分析为鉴定FgV1触发的信号传导和抗病毒反应的宿主调节因子提供了机会，并有助于理解FgV1与[具体物种]相互作用之间的复杂调控网络。
