Lu Shan, Zhang Haoyang, Guo Feng, Yang Yanfang, Shen Xiaorui, Chen Baoshan
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Ministry and Province Co-sponsored Collaborative Innovation Center for Sugarcane and Sugar Industry, Nanning, China.
Guangxi Key Laboratory of Sugarcane Biology, College of Agriculture, Guangxi University, Nanning, China.
Front Microbiol. 2022 Sep 20;13:954767. doi: 10.3389/fmicb.2022.954767. eCollection 2022.
The basidiomycete fungus is the causative agent of sugarcane smut disease. Mating between two strains of the opposite mating type is essential for filamentous growth and infection in sugarcane plants. However, the mechanisms underlying mating and pathogenicity are still not well understood. In this work we used gene disruption to investigate the role of , the gene encoding a kinase regulator in . Deletion of did not alter the haploid cell morphology or growth rate or tolerance to stress, but mutants with both alleles deleted lost mating ability and infectivity. Deletion of one allele in a pair with a wild-type strain resulted in impaired mating and reduced virulence. Transcriptome profiling revealed that about a third of genes underwent reprogramming in the wild types during mating. Although gene expression reprogramming occurred in the pairing of -null mutants, their transcriptomic profile differed significantly from that of the wild types, in which 625 genes differed from those present in the wild types that seemed to be among the required genes for a successful mating. These genes include those known to regulate mating and pathogenicity, such as components of the MAPK pathway and . Additionally, a total of 908 genes were differentially expressed in an out-of-control manner in the mutants. We conclude that SsUbc2 functions as a key factor to coordinate the reprogramming of gene expression at the global level and is essential for the transition from monokaryotic basidial growth to dikaryotic hyphal growth through mating.
担子菌是甘蔗黑穗病的病原体。两个相反交配型菌株之间的交配对于甘蔗植株中的丝状生长和感染至关重要。然而，交配和致病性的潜在机制仍未得到充分了解。在这项工作中，我们使用基因敲除来研究编码激酶调节因子的基因在中的作用。基因的缺失并未改变单倍体细胞形态、生长速率或对胁迫的耐受性，但两个等位基因均缺失的突变体失去了交配能力和感染性。与野生型菌株配对时，一对中一个等位基因的缺失导致交配受损和毒力降低。转录组分析表明，在交配过程中，野生型中约三分之一的基因发生了重编程。尽管在基因缺失突变体的配对中发生了基因表达重编程，但其转录组图谱与野生型有显著差异，其中625个基因与野生型中的基因不同，这些基因似乎是成功交配所需的基因之一。这些基因包括已知调节交配和致病性的基因，如丝裂原活化蛋白激酶（MAPK）途径的组分和。此外，共有908个基因在突变体中以失控的方式差异表达。我们得出结论，SsUbc2作为一个关键因子，在全局水平上协调基因表达的重编程，并且对于通过交配从单核担子生长向双核菌丝生长的转变至关重要。
