Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana

Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is...
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Autor*in:	Yezhang Ding [verfasserIn] Matthew R. Dommel [verfasserIn] Chenggang Wang [verfasserIn] Qi Li [verfasserIn] Qi Zhao [verfasserIn] Xudong Zhang [verfasserIn] Shaojun Dai [verfasserIn] Zhonglin Mou [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	non-expressor of pathogenesis-related (PR) genes1 systemic acquired resistance salicylic acid null mutant basal immunity CRISPR mutant

Übergeordnetes Werk:	In: Frontiers in Plant Science - Frontiers Media S.A., 2011, 11(2020)
Übergeordnetes Werk:	volume:11 ; year:2020

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fpls.2020.570422

Katalog-ID:	DOAJ034544135

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spelling	10.3389/fpls.2020.570422 doi (DE-627)DOAJ034544135 (DE-599)DOAJ2be9f7f03bdb4e8187571b5f4224b7a7 DE-627 ger DE-627 rakwb eng SB1-1110 Yezhang Ding verfasserin aut Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is unknown whether npr1-1 and npr1-3 are null mutants. Moreover, the NPR1 transcript levels are induced two- to threefold upon pathogen infection or salicylic acid (SA) treatment, but the biological relevance of the induction is unclear. Here, we used molecular and biochemical approaches including quantitative PCR, immunoblot analysis, site-directed mutagenesis, and CRISPR/Cas9-mediated gene editing to address these questions. We show that npr1-3 is a potential null mutant, whereas npr1-1 is not. We also demonstrated that a truncated npr1 protein longer than the hypothesized npr1-3 protein is not active in SA signaling. Furthermore, we revealed that TGACG-binding (TGA) factors are required for NPR1 induction, but the reverse TGA box in the 5’UTR of NPR1 is dispensable for the induction. Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. Moreover, as npr1-1 is not a null mutant, we recommend that future research should use npr1-3 and potential null T-DNA insertion mutants for dissecting NPR1’s function in various physiopathological processes. non-expressor of pathogenesis-related (PR) genes1 systemic acquired resistance salicylic acid null mutant basal immunity CRISPR mutant Plant culture Matthew R. Dommel verfasserin aut Chenggang Wang verfasserin aut Qi Li verfasserin aut Qi Zhao verfasserin aut Xudong Zhang verfasserin aut Shaojun Dai verfasserin aut Zhonglin Mou verfasserin aut In Frontiers in Plant Science Frontiers Media S.A., 2011 11(2020) (DE-627)662359240 (DE-600)2613694-6 1664462X nnns volume:11 year:2020 https://doi.org/10.3389/fpls.2020.570422 kostenfrei https://doaj.org/article/2be9f7f03bdb4e8187571b5f4224b7a7 kostenfrei https://www.frontiersin.org/article/10.3389/fpls.2020.570422/full kostenfrei https://doaj.org/toc/1664-462X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2003 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 11 2020
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allfieldsSound	10.3389/fpls.2020.570422 doi (DE-627)DOAJ034544135 (DE-599)DOAJ2be9f7f03bdb4e8187571b5f4224b7a7 DE-627 ger DE-627 rakwb eng SB1-1110 Yezhang Ding verfasserin aut Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is unknown whether npr1-1 and npr1-3 are null mutants. Moreover, the NPR1 transcript levels are induced two- to threefold upon pathogen infection or salicylic acid (SA) treatment, but the biological relevance of the induction is unclear. Here, we used molecular and biochemical approaches including quantitative PCR, immunoblot analysis, site-directed mutagenesis, and CRISPR/Cas9-mediated gene editing to address these questions. We show that npr1-3 is a potential null mutant, whereas npr1-1 is not. We also demonstrated that a truncated npr1 protein longer than the hypothesized npr1-3 protein is not active in SA signaling. Furthermore, we revealed that TGACG-binding (TGA) factors are required for NPR1 induction, but the reverse TGA box in the 5’UTR of NPR1 is dispensable for the induction. Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. Moreover, as npr1-1 is not a null mutant, we recommend that future research should use npr1-3 and potential null T-DNA insertion mutants for dissecting NPR1’s function in various physiopathological processes. non-expressor of pathogenesis-related (PR) genes1 systemic acquired resistance salicylic acid null mutant basal immunity CRISPR mutant Plant culture Matthew R. Dommel verfasserin aut Chenggang Wang verfasserin aut Qi Li verfasserin aut Qi Zhao verfasserin aut Xudong Zhang verfasserin aut Shaojun Dai verfasserin aut Zhonglin Mou verfasserin aut In Frontiers in Plant Science Frontiers Media S.A., 2011 11(2020) (DE-627)662359240 (DE-600)2613694-6 1664462X nnns volume:11 year:2020 https://doi.org/10.3389/fpls.2020.570422 kostenfrei https://doaj.org/article/2be9f7f03bdb4e8187571b5f4224b7a7 kostenfrei https://www.frontiersin.org/article/10.3389/fpls.2020.570422/full kostenfrei https://doaj.org/toc/1664-462X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2003 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 11 2020
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callnumber-first	S - Agriculture
author	Yezhang Ding
spellingShingle	Yezhang Ding misc SB1-1110 misc non-expressor of pathogenesis-related (PR) genes1 misc systemic acquired resistance misc salicylic acid misc null mutant misc basal immunity misc CRISPR mutant misc Plant culture Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana
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topic_title	SB1-1110 Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana non-expressor of pathogenesis-related (PR) genes1 systemic acquired resistance salicylic acid null mutant basal immunity CRISPR mutant
topic	misc SB1-1110 misc non-expressor of pathogenesis-related (PR) genes1 misc systemic acquired resistance misc salicylic acid misc null mutant misc basal immunity misc CRISPR mutant misc Plant culture
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title	Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana
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title_full	Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana
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title_sort	differential quantitative requirements for npr1 between basal immunity and systemic acquired resistance in arabidopsis thaliana
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title_auth	Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana
abstract	Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is unknown whether npr1-1 and npr1-3 are null mutants. Moreover, the NPR1 transcript levels are induced two- to threefold upon pathogen infection or salicylic acid (SA) treatment, but the biological relevance of the induction is unclear. Here, we used molecular and biochemical approaches including quantitative PCR, immunoblot analysis, site-directed mutagenesis, and CRISPR/Cas9-mediated gene editing to address these questions. We show that npr1-3 is a potential null mutant, whereas npr1-1 is not. We also demonstrated that a truncated npr1 protein longer than the hypothesized npr1-3 protein is not active in SA signaling. Furthermore, we revealed that TGACG-binding (TGA) factors are required for NPR1 induction, but the reverse TGA box in the 5’UTR of NPR1 is dispensable for the induction. Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. Moreover, as npr1-1 is not a null mutant, we recommend that future research should use npr1-3 and potential null T-DNA insertion mutants for dissecting NPR1’s function in various physiopathological processes.
abstractGer	Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is unknown whether npr1-1 and npr1-3 are null mutants. Moreover, the NPR1 transcript levels are induced two- to threefold upon pathogen infection or salicylic acid (SA) treatment, but the biological relevance of the induction is unclear. Here, we used molecular and biochemical approaches including quantitative PCR, immunoblot analysis, site-directed mutagenesis, and CRISPR/Cas9-mediated gene editing to address these questions. We show that npr1-3 is a potential null mutant, whereas npr1-1 is not. We also demonstrated that a truncated npr1 protein longer than the hypothesized npr1-3 protein is not active in SA signaling. Furthermore, we revealed that TGACG-binding (TGA) factors are required for NPR1 induction, but the reverse TGA box in the 5’UTR of NPR1 is dispensable for the induction. Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. Moreover, as npr1-1 is not a null mutant, we recommend that future research should use npr1-3 and potential null T-DNA insertion mutants for dissecting NPR1’s function in various physiopathological processes.
abstract_unstemmed	Non-expressor of pathogenesis-related (PR) genes1 (NPR1) is a key transcription coactivator of plant basal immunity and systemic acquired resistance (SAR). Two mutant alleles, npr1-1 and npr1-3, have been extensively used for dissecting the role of NPR1 in various signaling pathways. However, it is unknown whether npr1-1 and npr1-3 are null mutants. Moreover, the NPR1 transcript levels are induced two- to threefold upon pathogen infection or salicylic acid (SA) treatment, but the biological relevance of the induction is unclear. Here, we used molecular and biochemical approaches including quantitative PCR, immunoblot analysis, site-directed mutagenesis, and CRISPR/Cas9-mediated gene editing to address these questions. We show that npr1-3 is a potential null mutant, whereas npr1-1 is not. We also demonstrated that a truncated npr1 protein longer than the hypothesized npr1-3 protein is not active in SA signaling. Furthermore, we revealed that TGACG-binding (TGA) factors are required for NPR1 induction, but the reverse TGA box in the 5’UTR of NPR1 is dispensable for the induction. Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. Moreover, as npr1-1 is not a null mutant, we recommend that future research should use npr1-3 and potential null T-DNA insertion mutants for dissecting NPR1’s function in various physiopathological processes.
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title_short	Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana
url	https://doi.org/10.3389/fpls.2020.570422 https://doaj.org/article/2be9f7f03bdb4e8187571b5f4224b7a7 https://www.frontiersin.org/article/10.3389/fpls.2020.570422/full https://doaj.org/toc/1664-462X
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Finally, we show that full induction of NPR1 is required for basal immunity, but not for SAR, whereas sufficient basal transcription is essential for full-scale establishment of SAR. Our results indicate that induced transcript accumulation may be differentially required for different functions of a specific gene. 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Dommel</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Chenggang Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qi Li</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qi Zhao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Xudong Zhang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shaojun Dai</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhonglin 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Differential Quantitative Requirements for NPR1 Between Basal Immunity and Systemic Acquired Resistance in Arabidopsis thaliana

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