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   <subfield code="a">WetA and VosA are distinct regulators of conidiation capacity, conidial quality, and biological control potential of a fungal insect pathogen</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Fang Li, Han-Qiang Shi, Sheng-Hua Ying, Ming-Guang Feng]</subfield>
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   <subfield code="a">Many filamentous fungi produce only conidia for dispersal and survival in vitro or in vivo. Here, we show that the developmental regulator WetA and the velvet protein VosA are not only required for conidial maturation but indispensable for conidiation in Beauveria bassiana, a filamentous entomopathogen. Deletion of wetA or vosA resulted in more than 90% transcriptional depression of brlA and abaA, two activator genes in the central developmental pathway, during the critical period of conidiophore development and conidiation. Consequently, ΔwetA and ΔvosA strains lost 98% in and 88% of their conidiation capacities under optimal culture conditions, respectively. The conidia of ΔwetA showed more defective features than those of ΔvosA, including smaller size, lesser density, lower hydrophobicity, and impaired cell walls although intracellular trehalose content decreased more in the aging culture of ΔvosA than of ΔwetA. As a result, conidial sensitivity to cell wall perturbation was elevated in ΔwetA but unaffected in ΔvosA, which produced conidia more sensitive to the oxidant menadione and the wet-heat stress at 45°C. Both deletion mutants showed similar defects in conidial tolerance to high osmolarity or UV-B irradiation but no change in conidial sensitivity to the other oxidant H2O2 or the fungicide carbendazim. Moreover, ΔwetA lost more virulence to Galleria mellonella larvae than ΔvosA. All these phenotypical changes were restored by either wetA or vosA complementation. Taken together, WetA and VosA are indispensable for asexual development and contribute differentially to conidial quality and hence the biological control potential of B. bassiana against insect pests.</subfield>
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   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2015</subfield>
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   <subfield code="a">Li</subfield>
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   <subfield code="u">Institute of Microbiology, College of Life Sciences, Zhejiang University, 310058, Hangzhou, Zhejiang, People's Republic of China</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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