this with annotations you find in gene/protein databases, but these can be outdated or inaccurate. Falcon Edison Scientific Literature 31 citations 2 artifacts 2026-06-01T06:21:09.367219

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Research report: Arabidopsis thaliana NPR1 (UniProt P93002; At1g64280; NIM1/SAI1)

1) Verification of correct gene/protein identity

The target protein is Arabidopsis thaliana NPR1 (synonyms NIM1/SAI1), explicitly equated with UniProt P93002 in the retrieved literature, and described as a nucleo-cytoplasmic defense regulator containing a BTB/POZ domain and ankyrin repeats, matching the UniProt domain architecture provided in the prompt (goyal2024analysisofthe pages 26-29).

2) Key concepts and definitions (current understanding)

NONEXPRESSER OF PATHOGENESIS-RELATED GENES 1 (NPR1) is currently understood as a central node in salicylic acid (SA)-mediated immunity, functioning as a transcriptional co-regulator required for induction of SA-responsive defense genes such as PR1 and for systemic acquired resistance (SAR) (kim2023salicylicacidand pages 2-4, goyal2024analysisofthe pages 29-31). NPR1-family signaling is often conceptualized as a receptor/co-regulator module in which NPR1 (positive regulator) works alongside NPR3/NPR4 (negative regulators/SA receptors) to tune transcriptional output and protein turnover in response to SA concentrations (goyal2024analysisofthe pages 26-29, kim2023salicylicacidand pages 2-4).

Systemic acquired resistance (SAR) is a whole-plant immune state induced after local infection, requiring long-distance signaling and distal tissue reprogramming. A recent synthesis emphasizes that SA itself can function as a mobile signal with preferential apoplastic transport, and that distal immune activation includes NPR1-dependent transcriptional changes (kim2023salicylicacidand pages 4-5).

3) Molecular function, domains, and mechanism of action

3.1 Domain architecture and inferred biochemical role

NPR1 contains a BTB/POZ domain and four ankyrin repeats, consistent with a primary role in protein–protein interactions rather than DNA binding (goyal2024analysisofthe pages 26-29, kim2023salicylicacidand pages 2-4). Consistent with this, NPR1 (and NPR3/4) are described as lacking DNA-binding domains and acting through transcription factors, particularly the bZIP/TGA family (kim2023salicylicacidand pages 2-4).

3.2 Core transcriptional mechanism: partnering with TGA factors at PR promoters

NPR1 interacts with TGA transcription factors to activate SA-inducible promoters such as PR1, functioning as a coactivator that enables robust PR gene induction (goyal2024analysisofthe pages 34-37, kim2023salicylicacidand pages 2-4). A mechanistic layer relevant to functional annotation is that viral suppression of NPR1-mediated immunity can occur by disrupting the NPR1–TGA3 interaction (liu2023aplantrna pages 4-5). These concepts support the central annotation that NPR1’s primary molecular function is as a signal-dependent transcriptional co-regulator.

4) Subcellular localization and where NPR1 acts

NPR1 is best described as a nucleo-cytoplasmic protein whose function is executed primarily in the nucleus (transcriptional co-regulation), but whose activation state is controlled in the cytosol.

A current model supported by recent synthesis is:
- In uninduced conditions, NPR1 can exist as cytosolic oligomers stabilized by intermolecular disulfide bonds involving Cys82 and Cys216 (goyal2024analysisofthe pages 29-31).
- Immune induction with SA is associated with redox changes that reduce disulfides, producing monomeric NPR1 that translocates to the nucleus (goyal2024analysisofthe pages 29-31, goyal2024analysisofthe pages 95-98).
- Nuclear localization is described as necessary but not sufficient; an additional SA-dependent activation/conformational step is required for full transcriptional activation (goyal2024analysisofthe pages 29-31).

In a distinct physiological context—guard cells—NPR1 is implicated in systemic acquired stomatal immunity, consistent with NPR1 activity being relevant in specific cell types during SAR (guan2023roleofnpr1 pages 2-3).

5) Regulation of NPR1 (recent developments emphasized)

5.1 Redox and thiol-based regulation

Recent synthesis highlights thiol-switch regulation whereby oligomer–monomer transitions are mediated by cysteine redox state and modulated by S-nitrosylation at Cys156, which promotes oligomer accumulation by interfering with thioredoxin-mediated reduction (goyal2024analysisofthe pages 29-31). This positions NPR1 as a redox-sensitive immune regulator whose localization and activity are coupled to cellular redox status.

5.2 Phosphorylation–SUMOylation coupling and viral subversion (2023 primary study)

A major 2023 advance relevant to functional annotation is the description of NPR1 control by SUMO3-mediated SUMOylation and phosphorylation at Ser11/Ser15, and how a virus suppresses this module.

Liu et al. (Nature Communications, publication date 2023-06, URL https://doi.org/10.1038/s41467-023-39254-2) report that Turnip mosaic virus (TuMV) induces NPR1 SUMOylation and phosphorylation while activating SA–NPR1 output, but the viral RNA-dependent RNA polymerase NIb binds NPR1 (via NPR1’s SIM3 motif) to block interaction with SUMO3, thereby reducing NPR1 SUMOylation and suppressing downstream signaling (liu2023aplantrna pages 1-2, liu2023aplantrna pages 4-5). NIb also disrupts the NPR1–TGA3 interaction, providing a direct molecular route to transcriptional suppression (liu2023aplantrna pages 4-5). Mechanistically, NIb binding is supported by multiple interaction assays (Y2H, BiFC, Co-IP, pulldown) and mapped to NPR1’s central ankyrin (ANK) domain, with dependence on the SIM3 region (liu2023aplantrna pages 2-3).

This mechanism is summarized in the paper’s experimental figures and schematic model (Figure 3 and Figure 7 excerpts) showing NIb-mediated inhibition of NPR1 SUMOylation and downstream transcriptional activation circuitry (liu2023aplantrna media 090e7eb9, liu2023aplantrna media f98ddbf5).

5.3 Ubiquitin–proteasome control of nuclear NPR1 activity

A recent synthesis also emphasizes that proteasome-mediated turnover of nuclear NPR1 is integral to its coactivator function; ubiquitination is described as initiated at an N-terminal IκB-like phosphodegron requiring Ser11/Ser15 phosphorylation, and multiple E3/deubiquitinase components modulate NPR1 abundance and PR gene output (goyal2024analysisofthe pages 29-31). In parallel, the 2023 SA-transport/SAR review describes NPR3/NPR4 as SA receptors and CRL3 substrate adaptors that can mediate NPR1 polyubiquitination/degradation, with SA disrupting NPR1–NPR4 interaction and thereby stabilizing/activating NPR1 (kim2023salicylicacidand pages 4-5, kim2023salicylicacidand pages 2-4).

6) Pathways and biological processes involving NPR1

6.1 SA perception/signaling and systemic immunity

NPR1 is positioned as a core effector of SA signaling required for PR gene expression and broad-spectrum resistance (kim2023salicylicacidand pages 2-4). In the systemic context, SA transport and partitioning (apoplast, cuticle, transpiration effects) are integrated upstream of NPR1-dependent transcriptional responses that underlie SAR (kim2023salicylicacidand pages 4-5).

6.2 Systemic acquired stomatal immunity (2023 primary study)

Guan et al. (Plants, publication date 2023-05, URL https://doi.org/10.3390/plants12112137) provide evidence that NPR1 is required for systemic stomatal closure responses after priming/infection. In their experimental design, a local leaf is infiltrated with Pst DC3000 (or mock), then a distal leaf is challenged days later, and stomatal apertures are scored over time. The npr1-1 mutant failed to close stomata following pathogen exposure and showed increased systemic susceptibility compared with wild type (guan2023roleofnpr1 pages 2-3). Their quantitative label-free proteomics revealed large, genotype- and priming-dependent proteome shifts (e.g., 526 differentially abundant proteins in npr1-1 primed systemic leaves versus 204 in WT primed, with some proteins showing large changes such as ribosomal proteins up to log2FC ~6 and CAT2 ~log2FC 3.94) (guan2023roleofnpr1 pages 8-10). These data support NPR1 as a regulator linking systemic immune signals to guard-cell-associated defense physiology.

7) Recent developments and latest research (prioritizing 2023–2024)

Key 2023–2024 developments supported by the retrieved sources include:
- Direct viral targeting of NPR1’s PTM circuitry: NIb binding to NPR1 SIM3 blocks SUMO3 interaction/sumoylation and disrupts NPR1–TGA3, thereby subverting SA-mediated antiviral immunity (Liu 2023) (liu2023aplantrna pages 10-11, liu2023aplantrna pages 4-5).
- Integration of NPR1 into systemic stomatal immunity with proteome-scale data (Guan 2023), expanding NPR1’s well-known SAR transcriptional role into guard-cell-centered systemic defense physiology (guan2023roleofnpr1 pages 2-3, guan2023roleofnpr1 pages 8-10).
- Updated, review-level consensus on SA mobility and SA receptor modules: SA can move systemically via the apoplast; NPR3/NPR4 act as SA receptors/CRL3 adaptors controlling NPR1 stability and downstream transcriptional activation (Kim & Lim 2023) (kim2023salicylicacidand pages 4-5, kim2023salicylicacidand pages 2-4).
- Expanded, application-oriented review of SA-pathway activators emphasizing NPR1 as a key mechanistic node for chemical immunity priming and crop protection (Naz 2024) (naz2024thepastpresent pages 9-11, naz2024thepastpresent pages 2-5).

8) Current applications and real-world implementations

8.1 Chemical activators targeting the SA–NPR1 pathway

Naz et al. (Genes, publication date 2024-09, URL https://doi.org/10.3390/genes15091237) review multiple plant activators that induce SAR and are used in crop protection. BTH/ASM (acibenzolar-S-methyl; trade name “Bion”) is highlighted as a commercial SA analog developed for widespread crop use and supported by greenhouse/field evidence across many crop species and pathogens (naz2024thepastpresent pages 9-11). The review further notes activators whose induced resistance is genetically NPR1-dependent, e.g., compounds that fail to confer protection in npr1 mutants while remaining active in SA-depleted (NahG) contexts (naz2024thepastpresent pages 9-11, naz2024thepastpresent pages 11-13).

8.2 Quantified efficacy examples (activators/analogs)

Naz et al. also report quantified lesion-size reductions against TMV by SA analogs in tobacco, e.g., SA reduced lesion size by 80.3 ± 7.2%, while related chlorinated SA analogs showed similar magnitudes (e.g., 4-CSA: 76.0 ± 11.0%) (naz2024thepastpresent pages 11-13). While these data are not Arabidopsis-specific, they illustrate real-world screening/efficacy metrics used in SA/NPR1-targeting activator development.

8.3 Translational engineering in crops (NPR1-centered strategies)

A 2024 wheat systemic-resistance review reiterates that SA analogs (BTH/INA) can trigger SAR-like resistance in crops and notes that BTH-induced resistance can be partially NPR1-dependent, reinforcing NPR1’s translational importance as a target node for broad-spectrum resistance strategies (Zhao et al., Frontiers in Plant Science, publication date 2024-02, URL https://doi.org/10.3389/fpls.2024.1355178) (zhao2024enhancementofbroadspectrum pages 1-2).

9) Expert opinions and analysis (authoritative synthesis)

Recent reviews converge on a consistent “expert consensus” that NPR1 is a master regulator/coactivator for SA-mediated systemic immunity, whose output is controlled by (i) SA perception (including NPR3/4 receptor functions), (ii) protein stability/turnover via ubiquitin–proteasome pathways, and (iii) protein–protein interactions with TGAs and other regulators, enabling broad transcriptional reprogramming (kim2023salicylicacidand pages 2-4, goyal2024analysisofthe pages 29-31). Application-focused experts further argue that the same pathway logic underlies the success of commercial plant activators such as BTH/ASM in crop protection, and that improved mechanistic mapping of compound action sites within the pathway (including NPR1 dependence) is a key future direction (naz2024thepastpresent pages 9-11, naz2024thepastpresent pages 2-5).

10) Summary of key quantitative findings from recent studies

11) Concise functional annotation statement (usable for gene annotation)

NPR1 (P93002) is a salicylic-acid-responsive nucleo-cytoplasmic transcriptional co-regulator that controls SA-induced defense gene expression (e.g., PR1) and systemic acquired resistance by partnering with TGA transcription factors in the nucleus; its activity is gated by redox-dependent oligomer–monomer transitions, nuclear PTMs (SUMOylation/phosphorylation), and ubiquitin–proteasome turnover coordinated by SA receptor/adaptor proteins NPR3/NPR4 (goyal2024analysisofthe pages 29-31, kim2023salicylicacidand pages 2-4).

Category Key points Recent evidence (2023-2024) Notes
definition/concept • Arabidopsis NPR1 = AtNPR1 / NIM1 / SAI1, matching UniProt P93002 • Central salicylic acid (SA) signaling co-regulator/receptor required for PR gene induction and systemic acquired resistance (SAR) • Functions as a nucleo-cytoplasmic master regulator of defense transcription (goyal2024analysisofthe pages 26-29, goyal2024analysisofthe pages 29-31, goyal2024analysisofthe pages 23-26, saur2024arabidopsisnim1interacting1(nimin1) pages 1-4) Goyal 2024 dissertation excerpt; Kim & Lim 2023; Saur 2024 bioRxiv (goyal2024analysisofthe pages 26-29, kim2023salicylicacidand pages 4-5, saur2024arabidopsisnim1interacting1(nimin1) pages 1-4) Recent reviews/dissertation excerpts consistently support the classic Arabidopsis NPR1 identity; some mechanistic points remain model-dependent across studies.
domains • Contains BTB/POZ domain plus four ankyrin repeats consistent with protein-protein interaction roles • Includes nuclear localization signal and LENRV-like SA-binding motif • NIb interaction mapped to the central ankyrin domain and depends on SIM3 region for viral interference (goyal2024analysisofthe pages 29-31, goyal2024analysisofthe pages 26-29, liu2023aplantrna pages 2-3, saur2024arabidopsisnim1interacting1(nimin1) pages 1-4) Liu et al. 2023 Nature Communications; Goyal 2024 dissertation excerpt; Saur 2024 bioRxiv (goyal2024analysisofthe pages 29-31, liu2023aplantrna pages 2-3, saur2024arabidopsisnim1interacting1(nimin1) pages 1-4) Structural details are partly summarized indirectly from excerpts; Zhang 2025 notes 2022 structural work but the primary structure paper was not directly excerpted here (zhang2025salicylicacidand pages 10-11).
localization • In uninduced cells, NPR1 is largely in cytosolic oligomeric complexes • SA-associated redox change promotes monomerization and nuclear translocation • In guard cells/systemic leaves, NPR1 is important for stomatal immunity and distal defense responses (goyal2024analysisofthe pages 29-31, goyal2024analysisofthe pages 95-98, guan2023roleofnpr1 pages 2-3) Guan et al. 2023 Plants; Goyal 2024 dissertation excerpt (guan2023roleofnpr1 pages 2-3, goyal2024analysisofthe pages 29-31, goyal2024analysisofthe pages 95-98) Nuclear localization is necessary but not sufficient; excerpts note an additional SA-dependent conformational activation step (goyal2024analysisofthe pages 29-31).
regulation PTMs • Redox control: disulfide-linked oligomers involve Cys82/Cys216; S-nitrosylation at Cys156 favors oligomer accumulation • Phosphorylation: Ser11/Ser15 phosphodegron promotes transcriptional activity/turnover • SUMOylation/ubiquitination: SUMO3-linked activation interfaces with CRL3/CUL3-, UBE4-, and UBP6/7-mediated turnover (goyal2024analysisofthe pages 29-31, liu2023aplantrna pages 1-2, liu2023aplantrna pages 8-9, liu2023aplantrna pages 10-11, liu2023aplantrna pages 5-6) Liu et al. 2023 Nature Communications; Goyal 2024 dissertation excerpt (liu2023aplantrna pages 1-2, liu2023aplantrna pages 10-11, liu2023aplantrna pages 5-6, goyal2024analysisofthe pages 29-31) Strongest 2023 primary evidence here concerns viral suppression of NPR1 SUMOylation/phosphorylation; some broader PTM framework is synthesized in the dissertation excerpt rather than directly from each primary paper.
key partners • Interacts with TGA transcription factors to activate SA-responsive promoters such as PR1 • NPR3/NPR4 act as SA receptors/CRL3 substrate adaptors modulating NPR1 stability • NIMIN proteins bind NPR1 and can repress or tune SA responses; NIb from potyvirus targets NPR1 to suppress immunity (goyal2024analysisofthe pages 34-37, saur2024arabidopsisnim1interacting1(nimin1) pages 4-7, kim2023salicylicacidand pages 4-5, kim2023salicylicacidand pages 2-4, kim2023salicylicacidand pages 10-11, liu2023aplantrna pages 1-2) Kim & Lim 2023; Liu et al. 2023; Saur 2024 bioRxiv (goyal2024analysisofthe pages 34-37, saur2024arabidopsisnim1interacting1(nimin1) pages 4-7, kim2023salicylicacidand pages 4-5, kim2023salicylicacidand pages 2-4, liu2023aplantrna pages 1-2) NIMIN-related mechanisms in 2024 are from bioRxiv and should be treated as provisional until peer reviewed.
phenotypes/quantitative data • In npr1 mutants, viral accumulation increased ~1.8- to 2.1-fold versus WT in the TuMV pathosystem • TuMV infection induced PR1 >5-fold in WT, consistent with NPR1 pathway activation • In systemic stomatal immunity, proteomics found 335 WT-mock-only, 204 WT-primed-only, 337 npr1-1 mock, and 526 npr1-1 primed DAPs; some ribosomal protein changes reached log2FC ~6, catalase 2 ~3.94 log2FC (liu2023aplantrna pages 4-5, guan2023roleofnpr1 pages 8-10, guan2023roleofnpr1 pages 1-2) Liu et al. 2023 Nature Communications; Guan et al. 2023 Plants (liu2023aplantrna pages 4-5, guan2023roleofnpr1 pages 8-10, guan2023roleofnpr1 pages 1-2) Useful recent quantitative evidence exists, but many aperture/ROS numeric values were not present in the available excerpts.
applications • NPR1 is the canonical node leveraged by SA-pathway plant activators and SAR engineering • Commercial or field-relevant activators include BTH/ASM (Bion) and INA; several downstream activators fail in npr1 backgrounds, supporting NPR1 dependence • Translational relevance extends across crops including wheat, rice, tomato, cucumber, maize, cotton, soybean (naz2024thepastpresent pages 9-11, naz2024thepastpresent pages 11-13, naz2024thepastpresent pages 2-5, zhao2024enhancementofbroadspectrum pages 1-2) Naz et al. 2024 Genes; Zhao et al. 2024 Frontiers review (naz2024thepastpresent pages 9-11, naz2024thepastpresent pages 11-13, naz2024thepastpresent pages 2-5, zhao2024enhancementofbroadspectrum pages 1-2) Application evidence is largely review-based and often crop-translational rather than direct Arabidopsis functional annotation; however it shows how NPR1 knowledge is implemented in agriculture.

Table: This table summarizes the verified identity, molecular function, localization, regulatory mechanisms, partners, quantitative phenotypes, and applications of Arabidopsis thaliana NPR1 (UniProt P93002). It uses only the provided context snippets, emphasizing recent 2023-2024 evidence.

References

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  2. (kim2023salicylicacidand pages 2-4): Tae-Jin Kim and Gah-Hyun Lim. Salicylic acid and mobile regulators of systemic immunity in plants: transport and metabolism. Plants, 12:1013, Feb 2023. URL: https://doi.org/10.3390/plants12051013, doi:10.3390/plants12051013. This article has 63 citations.

  3. (goyal2024analysisofthe pages 29-31): Isha Goyal. Analysis of the regulation of ics1-independent sar gene expression by n-hydroxy-pipecolic acid. ArXiv, 2024. URL: https://doi.org/10.53846/goediss-10781, doi:10.53846/goediss-10781. This article has 0 citations.

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  11. (liu2023aplantrna media 090e7eb9): Jiahui Liu, Xiaoyun Wu, Yue Fang, Ye Liu, Esther Oreofe Bello, Yong Li, Ruyi Xiong, Yinzi Li, Zheng Qing Fu, Aiming Wang, and Xiaofei Cheng. A plant rna virus inhibits npr1 sumoylation and subverts npr1-mediated plant immunity. Nature Communications, Jun 2023. URL: https://doi.org/10.1038/s41467-023-39254-2, doi:10.1038/s41467-023-39254-2. This article has 65 citations and is from a highest quality peer-reviewed journal.

  12. (liu2023aplantrna media f98ddbf5): Jiahui Liu, Xiaoyun Wu, Yue Fang, Ye Liu, Esther Oreofe Bello, Yong Li, Ruyi Xiong, Yinzi Li, Zheng Qing Fu, Aiming Wang, and Xiaofei Cheng. A plant rna virus inhibits npr1 sumoylation and subverts npr1-mediated plant immunity. Nature Communications, Jun 2023. URL: https://doi.org/10.1038/s41467-023-39254-2, doi:10.1038/s41467-023-39254-2. This article has 65 citations and is from a highest quality peer-reviewed journal.

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  17. (naz2024thepastpresent pages 11-13): Misbah Naz, Dongqin Zhang, Kangcen Liao, Xulong Chen, Nazeer Ahmed, Delu Wang, Jing-Jiang Zhou, and Zhuo Chen. The past, present, and future of plant activators targeting the salicylic acid signaling pathway. Genes, 15:1237, Sep 2024. URL: https://doi.org/10.3390/genes15091237, doi:10.3390/genes15091237. This article has 27 citations.

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  23. (liu2023aplantrna pages 8-9): Jiahui Liu, Xiaoyun Wu, Yue Fang, Ye Liu, Esther Oreofe Bello, Yong Li, Ruyi Xiong, Yinzi Li, Zheng Qing Fu, Aiming Wang, and Xiaofei Cheng. A plant rna virus inhibits npr1 sumoylation and subverts npr1-mediated plant immunity. Nature Communications, Jun 2023. URL: https://doi.org/10.1038/s41467-023-39254-2, doi:10.1038/s41467-023-39254-2. This article has 65 citations and is from a highest quality peer-reviewed journal.

  24. (saur2024arabidopsisnim1interacting1(nimin1) pages 4-7): Mathias Saur, Kristin Steilner, Ashir Masroor, Philipp Hubel, Artur J.P. Pfitzner, and Ursula M. Pfitzner. Arabidopsis nim1-interacting1 (nimin1) is a multi-domain protein controlling transition from systemic acquired resistance (sar) to cell death. bioRxiv, Jul 2024. URL: https://doi.org/10.1101/2024.07.22.604541, doi:10.1101/2024.07.22.604541. This article has 0 citations.

  25. (kim2023salicylicacidand pages 10-11): Tae-Jin Kim and Gah-Hyun Lim. Salicylic acid and mobile regulators of systemic immunity in plants: transport and metabolism. Plants, 12:1013, Feb 2023. URL: https://doi.org/10.3390/plants12051013, doi:10.3390/plants12051013. This article has 63 citations.

  26. (guan2023roleofnpr1 pages 1-2): Qijie Guan, Lisa David, Riley Moran, Ivan Grela, Angelica Ortega, Peter Scott, Lindsey Warnock, and Sixue Chen. Role of npr1 in systemic acquired stomatal immunity. Plants, 12:2137, May 2023. URL: https://doi.org/10.3390/plants12112137, doi:10.3390/plants12112137. This article has 16 citations.

Artifacts

Citations

  1. goyal2024analysisofthe pages 26-29
  2. kim2023salicylicacidand pages 4-5
  3. kim2023salicylicacidand pages 2-4
  4. liu2023aplantrna pages 4-5
  5. goyal2024analysisofthe pages 29-31
  6. liu2023aplantrna pages 2-3
  7. naz2024thepastpresent pages 9-11
  8. naz2024thepastpresent pages 11-13
  9. zhao2024enhancementofbroadspectrum pages 1-2
  10. zhang2025salicylicacidand pages 10-11
  11. goyal2024analysisofthe pages 34-37
  12. goyal2024analysisofthe pages 95-98
  13. liu2023aplantrna pages 1-2
  14. liu2023aplantrna pages 10-11
  15. naz2024thepastpresent pages 2-5
  16. liu2023aplantrna pages 5-6
  17. goyal2024analysisofthe pages 23-26
  18. liu2023aplantrna pages 8-9
  19. kim2023salicylicacidand pages 10-11
  20. https://doi.org/10.1038/s41467-023-39254-2
  21. https://doi.org/10.3390/plants12112137
  22. https://doi.org/10.3390/genes15091237
  23. https://doi.org/10.3389/fpls.2024.1355178
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  25. https://doi.org/10.3390/plants12051013,
  26. https://doi.org/10.1038/s41467-023-39254-2,
  27. https://doi.org/10.3390/plants12112137,
  28. https://doi.org/10.3390/genes15091237,
  29. https://doi.org/10.3389/fpls.2024.1355178,
  30. https://doi.org/10.1101/2024.07.22.604541,
  31. https://doi.org/10.1093/hr/uhaf082,