Abstract
Csn5 is a subunit ofthe COP9/signalosome complex in model fungi. Here, we report heavier accumulation of orthologous Csn5 in the nucleus than in the cytoplasm and its indispensability to insect pathogenicity and virulence-related cellular events of Beauveria bassiana. Deletion of csn5 led to a 68% increase in intracellular ubiquitin accumulation and the dysregulation of 18 genes encoding ubiquitin-activating (E1), -conjugating (E2), and -ligating (E3) enzymes and ubiquitin-specific proteases, suggesting the role of Csn5 in balanced ubiquitination/deubiquitination. Consequently, the deletion mutant displayed abolished insect pathogenicity, marked reductions in conidial hydrophobicity and adherence to the insect cuticle, the abolished secretion of cuticle penetration-required enzymes, blocked haemocoel colonisation, and reduced conidiation capacity despite unaffected biomass accumulation. These phenotypes correlated well with sharply repressed or abolished expressions of key hydrophobin genes required for hydrophobin biosynthesis/assembly and of developmental activator genes essential for aerial conidiation and submerged blastospore production. In the mutant, increased sensitivities to heat shock and oxidative stress also correlated with reduced expression levels of several heat-responsive genes and decreased activities of antioxidant enzymes. Altogether, Csn5-reliant ubiquitination/deubiquitination balance coordinates the expression of those crucial genes and the quality control of functionally important enzymes, which are collectively essential for fungal pathogenicity, virulence-related cellular events, and asexual development.
Highlights
Hypocrealean insect pathogens are main sources of fungal insecticides, which are environment friendly and safe to apiculture [1,2]
Csn5 orthologues found in the NCBI databases of entomopathogenic and nonentomopathogenic fungi with the query of A. nidulans CsnE (Q5BBF1) were clustered into distinct clades consistent with host lineages in phylogeny and shared homology in structure (Figure S2)
Due to its role in transcriptional mediation [16] and the large number of Csn5-regulated genes identified from the transcriptomes of A. alternata and P. fici [39,40], our study focused on the possible role of Csn5 in the expressions of ubiquitin–proteasome system (UPS) genes as well as those required for asexual development; hydrophobin biosynthesis and stress response; and the quality/function control of those enzymes crucial for conidial adherence, cuticular penetration, and antioxidant activity
Summary
Hypocrealean insect pathogens are main sources of fungal insecticides, which are environment friendly and safe to apiculture [1,2]. The ubiquitination of target proteins is one of the posttranslational modification (PTM) mechanisms underlying the overall output [7,8] and is regulated by the ubiquitin–proteasome system (UPS), which comprises ubiquitin-activating (E1), -conjugating (E2) and -ligating (E3) enzymes and the ubiquitin-specific proteases (USPs) or deubiquitinases required for protein quality control and cell growth, division, differentiation, and development [9,10,11]. The COP9 (constitutive morphogenesis number 9 [12]) signalosome (CSN) is an eightubunit (Csn1–8/CsnA–H) protein complex that acts as a core player in PTMs such as ubiquitination/deubiquitination [13] and functions in diverse pathways essential for transcriptional regulation, DNA repair, the cell cycle, and cell differentiation and development across eukaryotes [14,15,16,17,18]. CRL activity is controlled through attachment/removal cycles of Nedd, which act as a switch for CRL-dependent ubiquitination for the activation or repression of target function [22]
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