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A conserved dimorphism-regulating histidine kinase controls the dimorphic switching in Paracoccidioides brasiliensis.
FEMS Yeast Res. 2016 08; 16(5)FY

Abstract

Paracoccidioides brasiliensis and P. lutzii, thermally dimorphic fungi, are the causative agents of paracoccidioidomycosis (PCM). Paracoccidioides infection occurs when conidia or mycelium fragments are inhaled by the host, which causes the Paracoccidioides cells to transition to the yeast form. The development of disease requires conidia inside the host alveoli to differentiate into yeast cells in a temperature-dependent manner. We describe the presence of a two-component signal transduction system in P. brasiliensis, which we investigated by expression analysis of a hypothetical protein gene (PADG_07579) that showed high similarity with the dimorphism-regulating histidine kinase (DRK1) gene of Blastomyces dermatitidis and Histoplasma capsulatum This gene was sensitive to environmental redox changes, which was demonstrated by a dose-dependent decrease in transcript levels after peroxide stimulation and a subtler decrease in transcript levels after NO stimulation. Furthermore, the higher PbDRK1 levels after treatment with increasing NaCl concentrations suggest that this histidine kinase can play a role as osmosensing. In the mycelium-yeast (M→Y) transition, PbDRK1 mRNA expression increased 14-fold after 24 h incubation at 37°C, consistent with similar observations in other virulent fungi. These results demonstrate that the PbDRK1 gene is differentially expressed during the dimorphic M→Y transition. Finally, when P. brasiliensis mycelium cells were exposed to a histidine kinase inhibitor and incubated at 37°C, there was a delay in the dimorphic M→Y transition, suggesting that histidine kinases could be targets of interest for PCM therapy.

Authors+Show Affiliations

Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Unidade José Alencar, Street São Nicolau, nº210, 4º floor, São Paulo 04023-900, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Unidade José Alencar, Street São Nicolau, nº210, 4º floor, São Paulo 04023-900, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Unidade José Alencar, Street São Nicolau, nº210, 4º floor, São Paulo 04023-900, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Unidade José Alencar, Street São Nicolau, nº210, 4º floor, São Paulo 04023-900, Brazil.Departamento de Ciências Farmacêuticas, Universidade Federal de São Paulo, Diadema 09913-030, São Paulo, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Unidade José Alencar, Street São Nicolau, nº210, 4º floor, São Paulo 04023-900, Brazil Departamento de Ciências Farmacêuticas, Universidade Federal de São Paulo, Diadema 09913-030, São Paulo, Brazil batista@unifesp.br.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27268997

Citation

Chaves, Alison F A., et al. "A Conserved Dimorphism-regulating Histidine Kinase Controls the Dimorphic Switching in Paracoccidioides Brasiliensis." FEMS Yeast Research, vol. 16, no. 5, 2016.
Chaves AF, Navarro MV, Castilho DG, et al. A conserved dimorphism-regulating histidine kinase controls the dimorphic switching in Paracoccidioides brasiliensis. FEMS Yeast Res. 2016;16(5).
Chaves, A. F., Navarro, M. V., Castilho, D. G., Calado, J. C., Conceição, P. M., & Batista, W. L. (2016). A conserved dimorphism-regulating histidine kinase controls the dimorphic switching in Paracoccidioides brasiliensis. FEMS Yeast Research, 16(5). https://doi.org/10.1093/femsyr/fow047
Chaves AF, et al. A Conserved Dimorphism-regulating Histidine Kinase Controls the Dimorphic Switching in Paracoccidioides Brasiliensis. FEMS Yeast Res. 2016;16(5) PubMed PMID: 27268997.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A conserved dimorphism-regulating histidine kinase controls the dimorphic switching in Paracoccidioides brasiliensis. AU - Chaves,Alison F A, AU - Navarro,Marina V, AU - Castilho,Daniele G, AU - Calado,Juliana C P, AU - Conceição,Palloma M, AU - Batista,Wagner L, Y1 - 2016/06/05/ PY - 2016/05/25/accepted PY - 2016/6/9/entrez PY - 2016/6/9/pubmed PY - 2017/8/2/medline KW - Paracoccidioides KW - dimorphism KW - histidine kinase KW - phosphorelay JF - FEMS yeast research JO - FEMS Yeast Res VL - 16 IS - 5 N2 - Paracoccidioides brasiliensis and P. lutzii, thermally dimorphic fungi, are the causative agents of paracoccidioidomycosis (PCM). Paracoccidioides infection occurs when conidia or mycelium fragments are inhaled by the host, which causes the Paracoccidioides cells to transition to the yeast form. The development of disease requires conidia inside the host alveoli to differentiate into yeast cells in a temperature-dependent manner. We describe the presence of a two-component signal transduction system in P. brasiliensis, which we investigated by expression analysis of a hypothetical protein gene (PADG_07579) that showed high similarity with the dimorphism-regulating histidine kinase (DRK1) gene of Blastomyces dermatitidis and Histoplasma capsulatum This gene was sensitive to environmental redox changes, which was demonstrated by a dose-dependent decrease in transcript levels after peroxide stimulation and a subtler decrease in transcript levels after NO stimulation. Furthermore, the higher PbDRK1 levels after treatment with increasing NaCl concentrations suggest that this histidine kinase can play a role as osmosensing. In the mycelium-yeast (M→Y) transition, PbDRK1 mRNA expression increased 14-fold after 24 h incubation at 37°C, consistent with similar observations in other virulent fungi. These results demonstrate that the PbDRK1 gene is differentially expressed during the dimorphic M→Y transition. Finally, when P. brasiliensis mycelium cells were exposed to a histidine kinase inhibitor and incubated at 37°C, there was a delay in the dimorphic M→Y transition, suggesting that histidine kinases could be targets of interest for PCM therapy. SN - 1567-1364 UR - https://www.unboundmedicine.com/medline/citation/27268997/A_conserved_dimorphism_regulating_histidine_kinase_controls_the_dimorphic_switching_in_Paracoccidioides_brasiliensis_ L2 - https://academic.oup.com/femsyr/article-lookup/doi/10.1093/femsyr/fow047 DB - PRIME DP - Unbound Medicine ER -