The Gene vepN Regulated by Global Regulatory Factor veA That Affects Aflatoxin Production, Morphological Development and Pathogenicity in Aspergillus flavus .
Jia XuMengqi JiangPeng WangQing KongPublished in: Toxins (2024)
Velvet (VeA), a light-regulated protein that shuttles between the cytoplasm and the nucleus, serves as a key global regulator of secondary metabolism in various Aspergillus species and plays a pivotal role in controlling multiple developmental processes. The gene vepN was chosen for further investigation through CHIP-seq analysis due to significant alterations in its interaction with VeA under varying conditions. This gene (AFLA_006970) contains a Septin-type guanine nucleotide-binding (G) domain, which has not been previously reported in Aspergillus flavus ( A. flavus ). The functional role of vepN in A. flavus was elucidated through the creation of a gene knockout mutant and a gene overexpression strain using a well-established dual-crossover recombinational technique. A comparison between the wild type (WT) and the Δ vepN mutant revealed distinct differences in morphology, reproductive capacity, colonization efficiency, and aflatoxin production. The mutant displayed reduced growth rate; dispersion of conidial heads; impaired cell wall integrity; and decreased sclerotia formation, colonization capacity, and aflatoxin levels. Notably, Δ vepN exhibited complete growth inhibition under specific stress conditions, highlighting the essential role of vepN in A. flavus . This study provides evidence that vepN positively influences aflatoxin production, morphological development, and pathogenicity in A. flavus .
Keyphrases
- wild type
- genome wide
- cell wall
- copy number
- genome wide identification
- transcription factor
- gene expression
- randomized controlled trial
- cell proliferation
- clinical trial
- single cell
- cystic fibrosis
- small molecule
- escherichia coli
- binding protein
- open label
- circulating tumor cells
- genome wide analysis
- double blind
- dna binding
- heat stress
- amino acid