Disease relevance of NPR1

• To investigate the role of NPR1 in monocots, we over-expressed the Arabidopsis NPR1 in rice and challenged the transgenic plants with Xanthomonas oryzae pv. oryzae (Xoo), the rice bacterial blight pathogen [1].
• Ethylene and jasmonic acid signaling affect the NPR1-independent expression of defense genes without impacting resistance to Pseudomonas syringae and Peronospora parasitica in the Arabidopsis ssi1 mutant [2].
• Plant growth-promoting rhizobacteria systemically protect Arabidopsis thaliana against Cucumber mosaic virus by a salicylic acid and NPR1-independent and jasmonic acid-dependent signaling pathway [3].
• The Arabidopsis NPR1 (nonexpresser of PR genes) gene was introduced into a tomato cultivar, which possesses heat-tolerance and resistance to tomato mosaic virus (ToMV) [4].

High impact information on NPR1

• These data provide a missing link between accumulation of SA and activation of NPR1 in the SAR signaling pathway [5].
• SAR induction results in accumulation of the signal molecule salicylic acid (SA), which induces defense gene expression via activation of NPR1 [5].
• The Arabidopsis NPR1 gene that controls systemic acquired resistance encodes a novel protein containing ankyrin repeats [6].
• The lesion in one npr1 mutant allele disrupted the ankyrin consensus sequence, suggesting that these repeats are important for NPR1 function [6].
• On the other hand, WRKY6 positively influenced the senescence- and pathogen defense-associated PR1 promoter activity, most likely involving NPR1 function [7].

Biological context of NPR1

• The Arabidopsis NPR1 protein is a key regulator of salicylic acid (SA)-mediated gene expression in systemic acquired resistance [8].
• In an attempt to identify proteins involved in SA-mediated signal transduction, we previously described the isolation of three novel genes encoding distinct albeit structurally related proteins designated NIMIN1 (for NIM1-INTERACTING1), NIMIN2, and NIMIN3 that interact with NPR1 in the yeast two-hybrid system [9].
• In vivo interaction between NPR1 and transcription factor TGA2 leads to salicylic acid-mediated gene activation in Arabidopsis [8].
• PR gene activity is regulated at the level of redox-dependent nuclear transport of NPR1 [9].
• This enhanced disease resistance is partially dependent on NPR1, can be in part complemented by either wild-type NPR3 or NPR4, and is not associated with an elevated level of salicylic acid [10].

Anatomical context of NPR1

• NPR1 modulates cross-talk between salicylate- and jasmonate-dependent defense pathways through a novel function in the cytosol [11].
• Interestingly, however, FB1-induced PCD does not require the SA signal transmitter NPR1, given that npr1-1 protoplasts display wild-type FB1 susceptibility [12].
• Because the levels of plastid complex lipid species containing hexadecatrienoic acid are depressed in all of the sfd ssi2 npr1 plants, we propose that these lipids are involved in the manifestation of the ssi2-conferred phenotypes [13].

Associations of NPR1 with chemical compounds

• We are systematically investigating the role of individual TGA factors in the transcriptional control of pathogenesis-related (PR) defense genes, whose expression is stimulated in leaves by salicylic acid (SA) through a stimulus pathway involving NPR1 [14].
• Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling pathway in which components from the jasmonate and ethylene response are engaged successively to trigger a defense reaction that, like SAR, is regulated by NPR1 [15].
• To gain a better understanding of NPR1 function, we conducted a yeast two-hybrid screening procedure and identified a differential interaction between NPR1 and all known members of the Arabidopsis TGA family of basic leucine zipper transcription factors [16].
• A mutation in the Arabidopsis gene ssi2/fab2, which encodes stearoyl-acyl carrier protein desaturase (S-ACP-DES), results in the reduction of oleic acid (18:1) levels in the mutant plants and also leads to the constitutive activation of NPR1-dependent and -independent defense responses [17].
• These results suggest that the ozone-induced expression of FAD7 gene requires SA, but not ethylene, JA, NPR1 and SID2 [18].

Physical interactions of NPR1

• These effects were dependent on the ability of NIMIN1 to interact with NPR1 [9].
• Coupled with observations that the DNA binding activity of TGA factors is deregulated in npr1 plants, the results suggest that NPR1-mediated DNA binding of TGA2 is critical for activation of defense genes [16].
• The Arabidopsis NPR1 disease resistance protein is a novel cofactor that confers redox regulation of DNA binding activity to the basic domain/leucine zipper transcription factor TGA1 [19].

Regulatory relationships of NPR1

• The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance [20].
• Potentiation of developmentally regulated defense responses by AtWRKY18 was not associated with enhanced biosynthesis of salicylic acid but required the disease resistance regulatory protein NPR1/NIM1 [21].
• PR1 expression is induced rapidly to a high level in the fungus-challenged spikes of the AtNPR1-expressing wheat [22].

Other interactions of NPR1

• Our results strongly suggest that NIMIN1 negatively regulates distinct functions of NPR1, providing a mechanism to modulate specific features of SAR [9].
• NPR1 has been shown to interact with three closely related TGA transcription factors-TGA2, TGA5, and TGA6-in yeast two-hybrid assays [23].
• We found increased GS accumulation in response to insect feeding, which required functional NPR1 and ETR1 but not COI1 or SA [24].
• Ozone-induced Expression of the Arabidopsis FAD7 Gene Requires Salicylic Acid, but not NPR1 and SID2 [18].
• Thus SA, NPR1, and PAD4 are required for the phenotypes [25].

Analytical, diagnostic and therapeutic context of NPR1

• The relevance of these findings to PR-1 expression was investigated by the use of chromatin immunoprecipitation, which demonstrated that in vivo these TGA factors are strongly recruited in an SA- and NPR1-dependent manner to the LS7-containing PR-1 promoter [14].
• In the electrophoretic mobility shift assay, NPR1 substantially increased the binding of TGA2 to its cognate promoter element (as-1) as well as to a positive salicylic acid-inducible element (LS7) and a negative element (LS5) in the promoter of the pathogenesis-related PR-1 gene [16].
• Here, we report the identification of another component, CPR 6, that may function with NPR1 in regulating PR gene expression [26].
• Furthermore, site-directed mutagenesis of TGA1 Cys-260 and Cys-266 enables the interaction with NPR1 in yeast and Arabidopsis [19].
• However, the SA signal transducer NPR1 was required only for constitutive PR-1 expression [27].

References