Three α-1,2-mannosyltransferases contribute differentially to conidiation, cell wall integrity, multistress tolerance and virulence of Beauveria bassiana

Gcn5‐dependent histone H3 acetylation and gene activity is required for the asexual development and virulence of Beauveria bassiana

“…The WT strain usually starts formation of zigzag rachises (conidiophores) and conidia in the 3‐day‐old SDAY culture initiated by spreading 100 μl of a 10 7 conidia ml −1 suspension per plate and incubated at 25°C in a light/dark (L:D) cycle of 12:12 h (Wang et al ., ). In this study, the WT strain gained a mean yield of 7 × 10 7 conidia cm −2 on day 4 and a maximum of 55 × 10 7 conidia cm −2 on day 8 under the same culture conditions (Fig.…”

“…Moreover, transcript levels of CDEP1 and CDEP2 , two cuticle‐degrading proteinase genes (Fang et al ., ; Xia et al ., ), were repressed respectively by 91% and 49% in the Δ gcn5 cultures, accompanied by differential repression of most genes encoding the family of Pr1 proteases (Fig. F), which are also likely involved in cuticle degradation (Wang et al ., ) but have been functionally unexplored yet in fungal insect pathogens. All of enzymatic and transcriptional changes were well restored in the complemented mutant.…”

“…The full‐length sequence was inserted into p0380‐sur‐gateway to exchange for the gateway fragment, yielding the complementary plasmid p0380‐sur‐gcn5. The target gene was deleted by homogenous recombination of the bar ‐separated cassette in the WT strain and complemented by ectopic integration of the sur cassette into Δ gcn5 mutant, as described previously (Wang et al ., ). Putative deletion and complement mutants were screened by the bar resistance to phosphinothricin (200 μg ml −1 ) and the sur resistance to chlorimuron ethyl (10 μg ml −1 ) respectively.…”

“…Previously, B. bassiana conidiation was abolished in the absence of brlA or abaA and greatly inhibited in the absence of wetA or vosA (Li et al ., ). The virulence of B. bassiana is a pleiotropic phenotype depending not only on the success of normal cuticle infection under the action of secreted cuticle‐degrading enzymes but also on the speeds of intrahaemocoel fungal proliferation and host mummification to death (Wang et al ., ; Zhu et al ., ; Chu et al ., ; Zhang et al ., ). The virulence‐related cellular events are of great diversity and complexity, such as dimorphic transition that turns cuticle‐penetrating hyphae into unicellular blastospores (also called hyphal bodies), which facilitate fungal proliferation by yeast‐like budding in host haemolymph and hence accelerate host mummification, and vice versa for fungal outgrowth at or near the time of host death and subsequent conidiation on the surfaces of insect cadavers.…”

Scanning Quadrupole Data-Independent Acquisition, Part B: Application to the Analysis of the Calcineurin-Interacting Proteins during Treatment of Aspergillus fumigatus with Azole and Echinocandin Antifungal Drugs

“…Mannosyltransferases play a crucial role in the modification of cell-wall proteins through the addition of N-linked or O-linked oligosaccharides and contribute to fungal virulence. 39 Ktr4 is responsible for glycosylation of cell-wall mannoproteins and cell-wall integrity, 40 and its deletion resulted in thinner cell walls and hypersensitivity cell-wall stress. Previous studies in our laboratory have revealed the localization of calcineurin at the hyphal tips and septa, 41 where active cell-wall synthesis occurs, lending support to the observed cell-wall and septation-related protein interactions in this study.…”