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.
Highlights
Plant systemic acquired resistance (SAR) is a long-lasting immune response against a broad-spectrum of pathogens (Durrant and Dong, 2004)
The epitopes recognized by the Non-expressor of pathogenesis-related (PR) genes1 (NPR1) antibody is uncertain, the antibody most likely would detect the truncated npr1-3 protein if it were expressed in the mutant plants
Glazebrook et al (2003) reported that, in response to Psm ES4326 infection, the npr1-3 mutation affected the expression of salicylic acid (SA)-regulated genes, whereas the npr1-1 mutation affected SA-related genes, and a much larger group of genes whose expression requires jasmonic acid (JA) and ET signaling
Summary
Plant systemic acquired resistance (SAR) is a long-lasting immune response against a broad-spectrum of pathogens (Durrant and Dong, 2004). The npr allele changed a highly conserved histidine (residue 334) in the third ankyrin-repeat to a tyrosine, whereas npr introduced a stop codon (residue 400) (Cao et al, 1997) Both npr and npr are null SAR mutants (Cao et al, 1997), they exhibited significant differences in relation to JA and ethylene (ET) signaling (Glazebrook et al, 2003; Spoel et al, 2003; Leon-Reyes et al, 2009; Canet et al, 2012). This assumption has never been proven and whether the speculated truncated npr protein exists or not is still an open question
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