WetA bridges cellular and chemical development in Aspergillus flavus

PLoS One. 2017 Jun 28;12(6):e0179571. doi: 10.1371/journal.pone.0179571. eCollection 2017.

Abstract

Bridging cellular reproduction and survival is essential for all life forms. Aspergillus fungi primarily reproduce by forming asexual spores called conidia, whose formation and maturation is governed by the central genetic regulatory circuit BrlA→AbaA→WetA. Here, we report that WetA is a multi-functional regulator that couples spore differentiation and survival, and governs proper chemical development in Aspergillus flavus. The deletion of wetA results in the formation of conidia with defective cell walls and no intra-cellular trehalose, leading to reduced stress tolerance, a rapid loss of viability, and disintegration of spores. WetA is also required for normal vegetative growth, hyphal branching, and production of aflatoxins. Targeted and genome-wide expression analyses reveal that WetA exerts feedback control of brlA and that 5,700 genes show altered mRNA levels in the mutant conidia. Functional category analyses of differentially expressed genes in ΔwetA RNA-seq data indicate that WetA contributes to spore integrity and maturity by properly regulating the metabolic pathways of trehalose, chitin, α-(1,3)-glucan, β-(1,3)-glucan, melanin, hydrophobins, and secondary metabolism more generally. Moreover, 160 genes predicted to encode transcription factors are differentially expressed by the absence of wetA, suggesting that WetA may play a global regulatory role in conidial development. Collectively, we present a comprehensive model for developmental control that bridges spore differentiation and survival in A. flavus.

MeSH terms

  • Aspergillus flavus / genetics
  • Aspergillus flavus / metabolism*
  • Cell Survival
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism*
  • Gene Expression Regulation, Fungal*
  • Genes, Fungal
  • Hyphae / metabolism
  • Reproduction, Asexual*

Substances

  • Fungal Proteins

Grants and funding

This work was supported by Hatch (WIS01665 and WIS01889) to JHY and the Intelligent Synthetic Biology Center of Global Frontier Projects (2015M3A6A8065838) to SCK and JHY. The sponsors or funders did not play any role in the design and conduct of the study, in the collection, analysis, and interpretation of the data, and in the preparation, review, or approval of the manuscript.