Effect of vacuolar ATPase subunit H (VmaH) on cellular pH, asexual cycle, stress tolerance and virulence in Beauveria bassiana

Zhu, Jing; Zhu, Xiao-Guan; Ying, Sheng‐Hua; Feng, Ming‐Guang

doi:10.1016/j.fgb.2016.12.004

Cited by 14 publications

(10 citation statements)

References 42 publications

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“…bassiana , when the vacuolar ATPase subunit H encoding gene was disrupted, conidia diameter was reduced by 16% when compared to the wild-type strain. Moreover, this mutant displayed significantly attenuated virulence against the Galleria mellonella larvae [41]. In both fungal phytopathogens B .…”

Section: Discussionmentioning

confidence: 99%

Heterotrimeric G-alpha subunits Gpa11 and Gpa12 define a transduction pathway that control spore size and virulence in Mucor circinelloides

et al. 2019

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Mucor circinelloides is one of the causal agents of mucormycosis, an emerging and high mortality rate fungal infection produced by asexual spores (sporangiospores) of fungi that belong to the order Mucorales. M. circinelloides has served as a model genetic system to understand the virulence mechanism of this infection. Although the G-protein signaling cascade plays crucial roles in virulence in many pathogenic fungi, its roles in Mucorales are yet to be elucidated. Previous study found that sporangiospore size and calcineurin are related to the virulence in Mucor, in which larger spores are more virulent in an animal mucormycosis model and loss of a calcineurin A catalytic subunit CnaA results in larger spore production and virulent phenotype. The M. circinelloides genome is known to harbor twelve gpa (gpa1 to gpa12) encoding G-protein alpha subunits and the transcripts of the gpa11 and gpa12 comprise nearly 72% of all twelve gpa genes transcript in spores. In this study we demonstrated that loss of function of Gpa11 and Gpa12 led to larger spore size associated with reduced activation of the calcineurin pathway. Interestingly, we found lower levels of the cnaA mRNAs in sporangiospores from the Δgpa12 and double Δgpa11/Δgpa12 mutant strains compared to wild-type and the ΔcnaA mutant had significantly lower gpa11 and gpa12 mRNA levels compared to wild-type. However, in contrast to the high virulence showed by the large spores of ΔcnaA, the spores from Δgpa11/Δgpa12 were avirulent and produced lower tissue invasion and cellular damage, suggesting that the gpa11 and gpa12 define a signal pathway with two branches. One of the branches controls spore size through regulation of calcineurin pathway, whereas virulences is controlled by an independent pathway. This virulence-related regulatory pathway could control the expression of genes involved in cellular responses important for virulence, since sporangiospores of Δgpa11/Δgpa12 were less resistant to oxidative stress and phagocytosis by macrophages than the ΔcnaA and wild-type strains. The characterization of this pathway could contribute to decipher the signals and mechanism used by Mucorales to produce mucormycosis.

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Section: Discussionmentioning

confidence: 99%

Heterotrimeric G-alpha subunits Gpa11 and Gpa12 define a transduction pathway that control spore size and virulence in Mucor circinelloides

et al. 2019

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“…The prominent contributors include the genes encoding three vacuole‐localized proteins Vlp1‐3 (41–57%), 112 transcription factor Som1 (52%), 113 phosphatase Cdc14 (50%), 114 Class II lysyl‐tRNA synthetase Krs (46%) 115 and multiprotein bridging factor 1 Mbf1 (40%) 116 . The remaining genes contribute 12–32% based on reduced LD 50 in the absence of each 117–124 . However, UVB LD 50 increased markedly by 18–23% in the absence of each of three other genes encoding the phosphatase Cdc25 120 and the histidine kinases HK6 (group VI) and HK10 (group X) in B. bassiana , 96 suggesting negative roles in fungal UV resistance akin to those mentioned in the TRX‐TRR and GRX‐GLR systems.…”

Section: Broad Molecular Basis Of Fungal Uv Resistancementioning

confidence: 99%

Molecular basis and regulatory mechanisms underlying fungal insecticides' resistance to solar ultraviolet irradiation

Tong

Feng

2021

Pest Management Science

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Resistance to solar ultraviolet (UV) irradiation is crucial for field‐persistent control efficacies of fungal formulations against arthropod pests, because their active ingredients are formulated conidia very sensitive to solar UV wavelengths. This review seeks to summarize advances in studies aiming to quantify, understand and improve conidial UV resistance. One focus of studies has been on the many sets of genes that have been revealed in the postgenomic era to contribute to or mediate UV resistance in the insect pathogens serving as main sources of fungal insecticides. Such genetic studies have unveiled the broad basis of UV‐resistant molecules including cytosolic solutes, cell wall components, various antioxidant enzymes, and numerous effectors and signaling proteins, that function in developmental, biosynthetic and stress‐responsive pathways. Another focus has been on the molecular basis and regulatory mechanisms underlying photorepair of UV‐induced DNA lesions and photoreactivation of UV‐impaired conidia. Studies have shed light upon a photoprotective mechanism depending on not only one or two photorepair‐required photolyases, but also two white collar proteins and other partners that play similar or more important roles in photorepair via interactions with photolyases. Research hotspots are suggested to explore a regulatory network of fungal photoprotection and to improve the development and application strategies of UV‐resistant fungal insecticides. © 2021 Society of Chemical Industry.

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“…This process has been evidently associated with the functions of many genes characterized in B. bassiana, such as those encoding the histone acetyltransferases Gcn5 and Mst2 (7, 9), the histone deacetylases Hos2 and Rpd3 (10, 11), the mitogen-activated protein kinase (MAPK) kinase Ste7 (12), the Na + /H + antiporter Nhx1 (13), the blue-light photoreceptor VVD (6), the vacuolar protein VLP4 (14) or ATPase subunit H VmaH (15), the lysyl-tRNA synthetase KRS (16), and the cyclophilin B CypB (17). Interestingly, these studied genes are also responsible for a correlation of dimorphic transition in vitro or in vivo with aerial conidiation and transcriptional activation of key activator genes in the central development pathway, as summarized in Table 1.…”

Section: Introductionmentioning

confidence: 99%

BrlA and AbaA Govern Virulence-Required Dimorphic Switch, Conidiation, and Pathogenicity in a Fungal Insect Pathogen

et al. 2019

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Dimorphic plant and human mycopathogens require a switch from the usual yeast growth to filamentous growth for host tissue penetration, and the switch is controlled by multiple signaling systems other than the central developmental pathway. Unlike these fungi, dimorphic insect mycopathogens usually grow by hyphal extension, infect the host by hyphal penetration through the insect cuticle, and switch to unicellular blastospores from the penetrating hyphae only after entry into the host hemocoel, where blastospore propagation by yeast-like budding accelerates host mummification. Here, we report a dependence of the virulence-required dimorphic transition on the central pathway activators BrlA and AbaA in Beauveria bassiana. Deletion of brlA or abaA abolished both aerial conidiation and submerged blastospore formation in vitro despite no negative impact on hyphal growth in various media, including a broth mimic of insect hemolymph. The hyphae of either deletion mutant lost insect pathogenicity through normal cuticle penetration, contrasting with a high infectivity of wild-type hyphae. The mutant hyphae injected into the host hemocoel failed to form blastospores, resulting in slower lethal action. Uncovered by transcriptomic analysis, several genes involved in host adhesion and cuticle degradation were sharply repressed in both deletion mutants versus wild type. However, almost all signaling genes homologous to those acting in the dimorphic switch of other fungi were not differentially expressed at a significant level and hence unlikely to be involved in shutting down the dimorphic switch of each deletion mutant. Therefore, like aerial conidiation, the submerged dimorphic switch in vitro and in vivo is a process of asexual development governed by the two central pathway activators in B. bassiana. IMPORTANCE Dimorphic insect mycopathogens infect the host by hyphal penetration through the host cuticle and switch from the penetrating hyphae to unicellular blastospores after entry into the host hemocoel, where blastospore propagation by yeast-like budding accelerates host mummification to death. The fungal virulence-required dimorphic switch is confirmed as a process of asexual development directly regulated by BrlA and AbaA, two key activators of the central developmental pathway in an insect mycopathogen. This finding unveils a novel mechanism distinct from the control of the dimorphic switch by multiple signaling systems other than the central developmental pathway in dimorphic plant and human mycopathogens, which switch from the usual yeast growth to filamentous growth required for pathogenicity through host tissue penetration.

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Effect of vacuolar ATPase subunit H (VmaH) on cellular pH, asexual cycle, stress tolerance and virulence in Beauveria bassiana

Cited by 14 publications

References 42 publications

Heterotrimeric G-alpha subunits Gpa11 and Gpa12 define a transduction pathway that control spore size and virulence in Mucor circinelloides

Heterotrimeric G-alpha subunits Gpa11 and Gpa12 define a transduction pathway that control spore size and virulence in Mucor circinelloides

Molecular basis and regulatory mechanisms underlying fungal insecticides' resistance to solar ultraviolet irradiation

BrlA and AbaA Govern Virulence-Required Dimorphic Switch, Conidiation, and Pathogenicity in a Fungal Insect Pathogen

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