Insect fungal pathogens secrete a cell wall-associated glucanase that acts to help avoid recognition by the host immune system.

Fungal insect pathogens have evolved diverse mechanisms to evade host immune recognition and defense responses. However, identification of fungal factors involved in host immune evasion during cuticular penetration and subsequent hemocoel colonization remains limited. Here, we report that the entomopathogenic fungus Beauveria bassiana expresses an endo-β-1,3-glucanase (BbEng1) that functions in helping cells evade insect immune recognition/responses. BbEng1 was specifically expressed during infection, in response to host cuticle and hemolymph, and in the presence of osmotic or oxidative stress. BbEng1 was localized to the fungal cell surface/ cell wall, where it acts to remodel the cell wall pathogen associated molecular patterns (PAMPs) that can trigger host defenses, thus facilitating fungal cell evasion of host immune defenses. BbEng1 was secreted where it could bind to fungal cells. Cell wall β-1,3-glucan levels were unchanged in ΔBbEng1 cells derived from in vitro growth media, but was elevated in hyphal bodies, whereas glucan levels were reduced in most cell types derived from the BbEng1 overexpressing strain (BbEng1OE). The BbEng1OE strain proliferated more rapidly in the host hemocoel and displayed higher virulence as compared to the wild type parent. Overexpression of their respective Eng1 homologs or of BbEng1 in the insect fungal pathogens, Metarhizium robertsii and M. acridum also resulted in increased virulence. Our data support a mechanism by which BbEng1 helps the fungal pathogen to evade host immune surveillance by decreasing cell wall glucan PAMPs, promoting successful fungal mycosis. Author summary: Fungal pathogens infect insects via penetration through the host cuticle and proliferation within the hemocoel. Important aspects of how the fungus evades host immune defenses remain poorly understood. Here, we report that a secreted / cell-wall associated endo-β-1,3-glucanase (BbEng1) expressed by Beuaveria bassiana during host infection acts to help the pathogen evade host immune responses by reducing levels of cell wall glucans that act as pathogen associated molecular patterns (PAMPs) recognized by host defenses that act to induce immune responses. Loss of BbEng1 did not alter cell wall glucan levels in cells derived from in vitro growth media, but elevated in hyphal bodies, whereas overexpression of BbEng1 decreased cell wall glucan contents, with the latter resulting in increased virulence. BbEng1 homologs were also shown to contribute to virulence in the insect fungal pathogens Metarhizium robertsii and M. acridum. These findings uncover a critical molecular determinant employed by fungal pathogens to help evade host recognition that would otherwise induce subsequent immune defense responses. [ABSTRACT FROM AUTHOR]