Expression of FUB-1 and FUB-11 as Toxic genes responsible for virulence during pathogenesis and combination of biocontrol agents in inhibition of Fusaric acid of Fusarium oxysporum causing Fusarium wilt of Arachis hypogaea L.

Ground nut (Arachis hypogaea L.) is one of the most important crops universally cultivated in many countries and India is the second largest producer of groundnut. Fusarium oxysporum is a soil borne and devastating fungal plant pathogen that causes Fusarium wilt in A. hypogaea. In fungi, the genes involved in secondary metabolite (SM) biosynthesis are often localized in close proximity in the genome, usually adjacent to each other, and are regulated in a co-ordinated manner. The biosynthetic gene cluster of SM encodes transcription factors, protein for transport and enzymes. Fusaric acid (FA) is a highly toxic SM derived from polyketide and is produced by several species belonging to the genus Fusarium which plays a significant role in disease development. A comparative genomic and transcriptomic analysis of the FA biosynthetic gene (FUB) cluster in A. hypogaea L. indicates that the FUB cluster is comprising 12 genes (FUB-1 to FUB-12). Among them, FUB-1 and FUB-11 are expressed significantly, and quantification by real-time polymerase chain reaction shows a 1.1-fold and 1.3-fold increase, respectively. RNA Transcriptome sequencing analysis of leaf samples infected with F. oxysporum and leaf samples treated with combinations of biocontrol agents (Trichoderma viride + Pseudomonas fluorescens) depicted 111 infected specific genes, 1162 treated specific genes, 33 up and downregulatory genes, and also the toxic levels of FA were significantly reduced (0.1-fold increase in FUB-1 and 0.3-fold increase in FUB-11 expression). Gene ontology and pathway analysis results shed light onto the genetic and biochemical mechanism for the identification of FUB genes associated with FA production in F. oxysporum infecting A. hypogaea L. and potential benefits of using combination treatments to suppress Fusarium wilt disease.