Cla4A, a Novel Regulator of Gene Expression Networks Required for Asexual and Insect-Pathogenic Lifecycles of .

Cla4, an orthologous p21-activated kinase crucial for non-entomopathogenic fungal lifestyles, has two paralogs (Cla4A/B) functionally unknown in hypocrealean entomopathogens. Here, we report a regulatory role of Cla4A in gene expression networks of required for asexual and entomopathogenic lifecycles while Cla4B is functionally redundant. The deletion of resulted in severe growth defects, reduced stress tolerance, delayed conidiation, altered conidiation mode, impaired conidial quality, and abolished pathogenicity through cuticular penetration, contrasting with no phenotype affected by deletion.

Characterization of BbKlf1 as a novel transcription factor vital for asexual and infection cycles of Beauveria bassiana.

The large family of C2H2-type zinc finger transcription factors (TFs) comprise the Kruppel-like factors (KLFs) that evolved relatively late in eukaryotes but remain unexplored in filamentous fungi. Here, we report that an orthologue (BbKlf1) of yeast Klf1 mediating cell wall integrity (CWI) is a wide-spectrum TF evidently localized in nucleus and cytoplasm in Beauveria bassiana. BbKlf1 features conserved domains and multiple DNA-binding motifs predicted to bind multiple promoter DNA fragments of target genes across asexual developmental and stress-responsive pathways.

Genome-Wide Insight into Profound Effect of Carbon Catabolite Repressor (Cre1) on the Insect-Pathogenic Lifecycle of .

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 's utilization of nutrients in insect integument and hemocoel.