Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<

<i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifun...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Jasper E. James [verfasserIn] Jacinta Santhanam [verfasserIn] Richard D. Cannon [verfasserIn] Erwin Lamping [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	FSSC SR AtrR

Übergeordnetes Werk:	In: Journal of Fungi - MDPI AG, 2015, 8(2022), 10, p 1070
Übergeordnetes Werk:	volume:8 ; year:2022 ; number:10, p 1070

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/jof8101070

Katalog-ID:	DOAJ020918658

Internformat


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allfields	10.3390/jof8101070 doi (DE-627)DOAJ020918658 (DE-599)DOAJb1921b5fe06b4ae596f1d3a0c0f75f25 DE-627 ger DE-627 rakwb eng QH301-705.5 Jasper E. James verfasserin aut Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria. FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR Biology (General) Jacinta Santhanam verfasserin aut Richard D. Cannon verfasserin aut Erwin Lamping verfasserin aut In Journal of Fungi MDPI AG, 2015 8(2022), 10, p 1070 (DE-627)796588538 (DE-600)2784229-0 2309608X nnns volume:8 year:2022 number:10, p 1070 https://doi.org/10.3390/jof8101070 kostenfrei https://doaj.org/article/b1921b5fe06b4ae596f1d3a0c0f75f25 kostenfrei https://www.mdpi.com/2309-608X/8/10/1070 kostenfrei https://doaj.org/toc/2309-608X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 10, p 1070
spelling	10.3390/jof8101070 doi (DE-627)DOAJ020918658 (DE-599)DOAJb1921b5fe06b4ae596f1d3a0c0f75f25 DE-627 ger DE-627 rakwb eng QH301-705.5 Jasper E. James verfasserin aut Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria. FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR Biology (General) Jacinta Santhanam verfasserin aut Richard D. Cannon verfasserin aut Erwin Lamping verfasserin aut In Journal of Fungi MDPI AG, 2015 8(2022), 10, p 1070 (DE-627)796588538 (DE-600)2784229-0 2309608X nnns volume:8 year:2022 number:10, p 1070 https://doi.org/10.3390/jof8101070 kostenfrei https://doaj.org/article/b1921b5fe06b4ae596f1d3a0c0f75f25 kostenfrei https://www.mdpi.com/2309-608X/8/10/1070 kostenfrei https://doaj.org/toc/2309-608X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 10, p 1070
allfields_unstemmed	10.3390/jof8101070 doi (DE-627)DOAJ020918658 (DE-599)DOAJb1921b5fe06b4ae596f1d3a0c0f75f25 DE-627 ger DE-627 rakwb eng QH301-705.5 Jasper E. James verfasserin aut Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria. FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR Biology (General) Jacinta Santhanam verfasserin aut Richard D. Cannon verfasserin aut Erwin Lamping verfasserin aut In Journal of Fungi MDPI AG, 2015 8(2022), 10, p 1070 (DE-627)796588538 (DE-600)2784229-0 2309608X nnns volume:8 year:2022 number:10, p 1070 https://doi.org/10.3390/jof8101070 kostenfrei https://doaj.org/article/b1921b5fe06b4ae596f1d3a0c0f75f25 kostenfrei https://www.mdpi.com/2309-608X/8/10/1070 kostenfrei https://doaj.org/toc/2309-608X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 10, p 1070
allfieldsGer	10.3390/jof8101070 doi (DE-627)DOAJ020918658 (DE-599)DOAJb1921b5fe06b4ae596f1d3a0c0f75f25 DE-627 ger DE-627 rakwb eng QH301-705.5 Jasper E. James verfasserin aut Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria. FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR Biology (General) Jacinta Santhanam verfasserin aut Richard D. Cannon verfasserin aut Erwin Lamping verfasserin aut In Journal of Fungi MDPI AG, 2015 8(2022), 10, p 1070 (DE-627)796588538 (DE-600)2784229-0 2309608X nnns volume:8 year:2022 number:10, p 1070 https://doi.org/10.3390/jof8101070 kostenfrei https://doaj.org/article/b1921b5fe06b4ae596f1d3a0c0f75f25 kostenfrei https://www.mdpi.com/2309-608X/8/10/1070 kostenfrei https://doaj.org/toc/2309-608X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 10, p 1070
allfieldsSound	10.3390/jof8101070 doi (DE-627)DOAJ020918658 (DE-599)DOAJb1921b5fe06b4ae596f1d3a0c0f75f25 DE-627 ger DE-627 rakwb eng QH301-705.5 Jasper E. James verfasserin aut Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria. FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR Biology (General) Jacinta Santhanam verfasserin aut Richard D. Cannon verfasserin aut Erwin Lamping verfasserin aut In Journal of Fungi MDPI AG, 2015 8(2022), 10, p 1070 (DE-627)796588538 (DE-600)2784229-0 2309608X nnns volume:8 year:2022 number:10, p 1070 https://doi.org/10.3390/jof8101070 kostenfrei https://doaj.org/article/b1921b5fe06b4ae596f1d3a0c0f75f25 kostenfrei https://www.mdpi.com/2309-608X/8/10/1070 kostenfrei https://doaj.org/toc/2309-608X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 10, p 1070
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spellingShingle	Jasper E. James misc QH301-705.5 misc FSSC misc <i<cyp51</i< misc <i<erg6</i< misc <i<ebp1</i< misc SR misc AtrR misc Biology (General) Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<
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topic_title	QH301-705.5 Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i< FSSC <i<cyp51</i< <i<erg6</i< <i<ebp1</i< SR AtrR
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title	Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<
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title_full	Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<
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title_sort	voriconazole treatment induces a conserved sterol/pleiotropic drug resistance regulatory network, including an alternative ergosterol biosynthesis pathway, in the clinically important fssc species, <i<fusarium keratoplasticum</i<
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title_auth	Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<
abstract	<i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria.
abstractGer	<i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria.
abstract_unstemmed	<i<Fusarium keratoplasticum</i< is the <i<Fusarium</i< species most commonly associated with human infections (fusariosis). Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria.
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title_short	Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<
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Antifungal treatment of fusariosis is often hampered by limited treatment options due to resistance towards azole antifungals. The mechanisms of antifungal resistance and sterol biosynthesis in fusaria are poorly understood. Therefore, in this study we assessed the transcriptional response of <i<F. keratoplasticum</i< when exposed to voriconazole. Our results revealed a group of dramatically upregulated ergosterol biosynthesis gene duplicates, most notably <i<erg6A</i< (912-fold), <i<cyp51A</i< (52-fold) and <i<ebp1</i< (20-fold), which are likely part of an alternative ergosterol biosynthesis salvage pathway. The presence of human cholesterol biosynthesis gene homologs in <i<F. keratoplasticum</i< (<i<ebp1</i<, <i<dhcr7</i< and <i<dhcr24_1</i<, <i<dhcr24_2</i< and <i<dhcr24_3</i<) suggests that additional sterol biosynthesis pathways may be induced in fusaria under other growth conditions or during host invasion. Voriconazole also induced the expression of a number of ABC efflux pumps. Further investigations suggested that the highly conserved master regulator of ergosterol biosynthesis, FkSR, and the pleiotropic drug resistance network that induces zinc-cluster transcription factor FkAtrR coordinate the response of FSSC species to azole antifungal exposure. In-depth genome mining also helped clarify the ergosterol biosynthesis pathways of moulds and provided a better understanding of antifungal drug resistance mechanisms in fusaria.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">FSSC</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<cyp51</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<erg6</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<ebp1</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">SR</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">AtrR</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biology (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jacinta Santhanam</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Richard D. 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Voriconazole Treatment Induces a Conserved Sterol/Pleiotropic Drug Resistance Regulatory Network, including an Alternative Ergosterol Biosynthesis Pathway, in the Clinically Important FSSC Species, <i<Fusarium keratoplasticum</i<

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