Abstract
Carbon catabolite repression (CCR) is critical for the preferential utilization of glucose derived from environmental carbon sources and regulated by carbon catabolite repressor A (Cre1/CreA) in filamentous fungi. However, a role of Cre1-mediated CCR in insect-pathogenic fungal utilization of host nutrients during normal cuticle infection (NCI) and hemocoel colonization remains explored insufficiently. Here, we report an indispensability of Cre1 for Beauveria bassiana’s utilization of nutrients in insect integument and hemocoel. Deletion of cre1 resulted in severe defects in radial growth on various media, hypersensitivity to oxidative stress, abolished pathogenicity via NCI or intrahemocoel injection (cuticle-bypassing infection) but no change in conidial hydrophobicity and adherence to insect cuticle. Markedly reduced biomass accumulation in the Δcre1 cultures was directly causative of severe defect in aerial conidiation and reduced secretion of various cuticle-degrading enzymes. The majority (1117) of 1881 dysregulated genes identified from the Δcre1 versus wild-type cultures were significantly downregulated, leading to substantial repression of many enriched function terms and pathways, particularly those involved in carbon and nitrogen metabolisms, cuticle degradation, antioxidant response, cellular transport and homeostasis, and direct/indirect gene mediation. These findings offer a novel insight into profound effect of Cre1 on the insect-pathogenic lifestyle of B. bassiana.
Highlights
Published: 23 October 2021Fungal growth and development rely upon the utilization of nutrients in the forms of environmental carbon and nitrogen sources
Bioinformatic information of Cre1 (NCBI accession code: EJP65725; 385 amino acids) in this study is identical to BbCreA investigated previously [37]
Images, the green fluorescence-tagged Cre1-GFP fusion protein accumulated in both cytoplasm and nuclei of hyphal cells from the culture grown in SDBY containing glucose, 3
Summary
Fungal growth and development rely upon the utilization of nutrients in the forms of environmental carbon and nitrogen sources. CCR is regulated by three transcription factors (Mig1–3), which feature DNA-binding Cys His zinc-finger motifs and mediate the expression of glucose-repressed genes vectoring Mig-binding sites in their promoter regions [1,2,3]. The nucleocytoplasmic shuttling of Mig is controlled by AMP-activated protein kinase Snf1p/SnfA [5,6], and by hexose kinase Hxk in the presence of glucose and mannose and by Hxk or Hxk in the presence of fructose [7]. The Mig orthologue Scr mediates many genes involved in carbon metabolism, hexose uptake, gluconeogenesis and tricarboxylic acid (TCA) cycle [8]
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