The NPR1 ortholog PhaNPR1 is required for the induction of PhaPR1 in Phalaenopsis aphroditeReportar como inadecuado




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Botanical Studies

, 54:31

Molecular Biology

Abstract

BackgroundSystematic acquired resistance SAR is an effective broad-spectrum defense mechanism that confers long-lasting protection against biotrophic pathogens trough defense related salicylic acid SA signaling. Genes involved in SAR have been extensively studied in dicot plants; however, remains largely unresolved in monocot plants. NPR1, an evolutionary conserved gene, plays a central role in SAR, and PR-1 is widely used as a marker for effective SA signaling.

ResultsWe identified NPR1 and PR-1 homologous genes, PhaNPR1 and PhaPR1, from an economically important orchid, Phalaenopsis aphrodite, and characterized their roles in SA signaling and Cymbidium mosaic virus CymMV resistance. A phylogenetic analysis of NPR1 homologs showed that these genes appear to have evolved before angiospermy. Similar to Arabidopsis NPR1, PhaNPR1 was only moderately induced upon SA treatment and CymMV infection. Although PhaPR1 shows only 36% identity with AtPR1, its promoter shared conserved elements with those of other PR-1 genes, and it was induced upon SA treatment and CymMV infection. After CymMV infection, silencing on PhaNPR1 also reduced PhaPR1 expression; however, CymMV accumulation was not affected.

ConclusionsIn conclusion, after virus infection, PhaNPR1 is required for PhaPR1 induction, but plays little role in defense against CymMV.

KeywordsNPR1 PR1 Phalaenopsis aphrodite Salicylic acid Systemic acquired resistance AbbreviationsBOPBLADE-ON-PETIOLE

BTHbenzo-1,2,3-thiadiazole-7-carbothioic acid S-methyl ester

CymMVCymbidium mosaic virus

GSPGene-specific primer

NPR1NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1

ORFOpen reading frame

PR-1PATHOGENESIS-RELATED GENES -1

RACERapid amplification of cDNA ends

SARSystematic acquired resistance.

Electronic supplementary materialThe online version of this article doi:10.1186-1999-3110-54-31 contains supplementary material, which is available to authorized users.

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Autor: Jen-Chih Chen - Hsiang-Chia Lu - Cheng-En Chen - Hua-Fang Hsu - Hong-Hwa Chen - Hsin-Hung Yeh

Fuente: https://link.springer.com/







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