Functional annotation of *Arabidopsis thaliana* MYB51 Falcon Edison Scientific Literature 32 citations 2 artifacts 2026-10-02T06:45:26.070342

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Functional annotation of Arabidopsis thaliana MYB51

Identity and principal function

The target is Arabidopsis thaliana MYB51/HIG1, locus At1g18570, corresponding to the supplied UniProt accession O49782—not a similarly named gene in another species. The original locus-specific study identified At1g18570 as HIGH INDOLIC GLUCOSINOLATE 1 and classified its 352-amino-acid product as a subgroup-12 R2R3-MYB transcription factor. Its paired MYB DNA-binding repeats agree with the MYB/SANT-related domains specified in the query; the broad “homeodomain-like” annotation should not be mistaken for evidence that it is a classical homeobox protein. (gigolashvili2007thetranscriptionfactor pages 2-3, berger2007theroleofa pages 34-39)

MYB51’s primary function is transcriptional control of tryptophan-derived indole glucosinolate biosynthesis, particularly in shoots and during some immune responses. It is not an enzyme or a metabolite transporter: it has no assigned catalytic reaction, chemical substrate specificity, or transported substrate. Its experimentally supported molecular targets are promoter regions of biosynthetic genes; the metabolic reactions themselves are catalyzed by the enzymes whose expression it regulates. (gigolashvili2007thetranscriptionfactor pages 2-3, barco2020hierarchicalanddynamic pages 6-7, frerigmann2014myb34myb51and pages 3-4)

Molecular mechanism and pathway position

Indole glucosinolates are sulfur-containing specialized metabolites derived from tryptophan. CYP79B2 and CYP79B3 catalyze conversion of tryptophan into indole-3-acetaldoxime (IAOx), a branch-point precursor also used in other indolic defense pathways. CYP83B1 channels IAOx toward the indole-glucosinolate core, leading to indol-3-ylmethyl glucosinolate (I3M, glucobrassicin); downstream modification produces, among other compounds, 4-methoxy-I3M. MYB51 controls flux into and through this branch by regulating gene expression, rather than performing any of these conversions itself. (frerigmann2014myb34myb51and pages 3-4, barco2020hierarchicalanddynamic pages 2-4, barco2020hierarchicalanddynamic pages 6-7)

The distinction between promoter activation and demonstrated chromatin occupancy matters. In 2007, MYB51 activated reporter promoters of DHS1, TSB1, CYP79B2, CYP79B3, CYP83B1 and AtST5a; ASA1 was not activated. These reporter assays established transcriptional capacity but did not alone prove physical promoter occupancy. In pathogen-elicited Arabidopsis seedlings, a 2020 chromatin-immunoprecipitation study subsequently found greater than tenfold MYB51 enrichment at proximal MYB-responsive regions of CYP79B2, CYP79B3 and CYP83B1. Its promoter maps and ChIP results directly support these three loci as in-vivo chromatin-associated targets; SUR1 expression responded to MYB51, but none of the four tested SUR1 promoter regions showed MYB51 occupancy, favoring indirect regulation there. ChIP demonstrates occupancy in plant chromatin, not, by itself, a purified-protein binding affinity or an exclusive consensus sequence. (gigolashvili2007thetranscriptionfactor pages 3-5, barco2020hierarchicalanddynamic pages 6-7, barco2020hierarchicalanddynamic media c75a5469)

The following summary separates directly supported promoter effects from downstream metabolic consequences. (gigolashvili2007thetranscriptionfactor pages 3-5, barco2020hierarchicalanddynamic pages 7-10, barco2020hierarchicalanddynamic pages 6-7)

Target/pathway Experimental evidence in Arabidopsis thaliana AtMYB51/HIG1 Regulatory direction Source
CYP79B2 and CYP79B3 — Trp → indole-3-acetaldoxime entry step Promoter–GUS assays showed MYB51-dependent transactivation in 2007. During Pseudomonas syringae avrRpm1 elicitation, MYB51 restored reduced expression in myb51 myb122; ChIP–PCR showed greater than 10-fold enrichment at proximal SMRE-containing promoter regions. ChIP demonstrates in-vivo chromatin occupancy, not purified-protein sequence-specific binding. Direct activation Gigolashvili et al., 2007; Barco and Clay, 2020 (gigolashvili2007thetranscriptionfactor pages 3-5, barco2020hierarchicalanddynamic pages 6-7, barco2020hierarchicalanddynamic media c75a5469)
CYP83B1 — commitment toward indole-glucosinolate synthesis Promoter–GUS transactivation was reported in 2007. Pathogen-elicited ChIP–PCR in 2020 detected greater than 10-fold enrichment at a proximal SMRE-containing promoter region, with MYB51-dependent restoration of transcript abundance. Direct activation Gigolashvili et al., 2007; Barco and Clay, 2020 (gigolashvili2007thetranscriptionfactor pages 3-5, barco2020hierarchicalanddynamic pages 6-7, barco2020hierarchicalanddynamic media c75a5469)
SUR1 — core glucosinolate C–S lyase step SUR1 expression decreased in myb51 myb122 and was restored by induced MYB51, but MYB51 did not occupy any of four tested SMRE-containing SUR1 promoter regions by ChIP–PCR. Indirect activation Barco and Clay, 2020 (barco2020hierarchicalanddynamic pages 6-7)
CYP82C2 — ICN → 4OH-ICN branch CYP82C2 expression was 3.5-fold higher in myb51 myb122 after pathogen elicitation and returned toward wild-type levels after MYB51 induction. MYB51 showed greater than 10-fold ChIP enrichment at two SMRE-containing promoter regions. Direct repression Barco and Clay, 2020 (barco2020hierarchicalanddynamic pages 7-10)
CYP71A12, CYP71A13 and CYP71B15/PAD3 — 4OH-ICN and camalexin branches MYB51 induction did not activate CYP71A12 or CYP71A13, and prior assays did not support activation of PAD3. Effects on camalexin and 4OH-ICN therefore arise chiefly through upstream flux control rather than demonstrated direct targeting. BES1 physically interacts with MYB51 and suppresses MYB51-driven CYP79B3 and UGT74B1 reporters, adding a negative regulatory layer. No demonstrated direct activation; downstream effects are indirect and context-dependent Barco and Clay, 2020; Liao et al., 2020 (barco2020hierarchicalanddynamic pages 6-7, liao2020brassinosteroidsantagonizejasmonateactivated pages 19-25)

Table: Direct and indirect molecular targets of Arabidopsis At1g18570/MYB51, separated by evidence type and regulatory direction. Chromatin occupancy is distinguished from purified-protein DNA-binding evidence.

MYB51 is not invariably an activator. Under effector-triggered immunity elicited by Pseudomonas syringae carrying avrRpm1, MYB51 occupied MYB-responsive regions of CYP82C2 and repressed its expression; CYP82C2 transcripts were 3.5-fold higher in myb51 myb122 than in wild type. CYP82C2 participates in production of 4-hydroxy-indole-3-carbonylnitrile (4OH-ICN). Thus MYB51 can promote precursor supply via CYP79B2/B3 while restraining this particular downstream branch via CYP82C2. In the same study, evidence did not support MYB51 directly activating the tested downstream camalexin or 4OH-ICN genes CYP71A12, CYP71A13 or CYP71B15/PAD3. (barco2020hierarchicalanddynamic pages 7-10, barco2020hierarchicalanddynamic pages 6-7)

Where the protein acts

Subcellular site: nucleus. Full-length MYB51–GFP accumulated in nuclei of tobacco BY2 protoplasts, cultured Arabidopsis cells and transiently transformed Arabidopsis leaves, consistent with a protein acting on nuclear gene transcription. The proposed basic amino-acid stretch KKRLIKK is a candidate localization signal, not a separately demonstrated import mechanism. Promoter-reporter experiments detected MYB51 expression in vascular-associated regions as well as leaf mesophyll, young-leaf pavement cells and trichomes; these expression territories should not be confused with additional protein compartments. The protein’s established functional site is the nucleus, not the chloroplast, glucosinolate storage compartment or extracellular space. (gigolashvili2007thetranscriptionfactor pages 2-3, gigolashvili2007thetranscriptionfactor pages 12-13)

Genetic, metabolic and physiological evidence

Activation-tagged HIG1-1D plants accumulated approximately six times as much I3M as wild type; independent constitutive MYB51-overexpression lines accumulated three- to eightfold as much. Other indolic glucosinolates, including 4-methoxy-I3M and 1-methoxy-I3M, also rose. Total glucosinolates increased by up to threefold, whereas the hig1-1 loss-of-function line had total glucosinolates at approximately one-third of wild-type levels. These are genotype- and growth-condition-specific results, not universal effect sizes; the same original study also noted changes in an aliphatic glucosinolate, so MYB51 should not be described as metabolically insulated from the rest of glucosinolate metabolism. (gigolashvili2007thetranscriptionfactor pages 2-3)

Comparative Arabidopsis mutant analyses clarified redundancy: MYB51 is particularly important for indole glucosinolate production in shoots; MYB34 has the stronger basal role in roots; MYB122 contributes more modestly. The myb34 myb51 myb122 triple mutant lacked detectable indole glucosinolates under the study’s standard conditions. With hormone treatments, MYB51 was the central regulator of the indole-glucosinolate response to salicylic acid and ethylene, whereas MYB34 was more important under abscisic acid and jasmonate treatments. These are relative roles, not claims that individual hormones act exclusively through one factor. (frerigmann2014myb34myb51and pages 3-4, frerigmann2014myb34myb51and pages 11-12)

The defense phenotype has direct experimental support. In a dual-choice leaf-feeding assay with the generalist herbivore Spodoptera exigua (20 larvae per comparison), larvae avoided high-indolic-glucosinolate HIG1-1D tissue compared with wild type (P = 0.0026) and hig1-1 (P = 0.0113); wild type versus hig1-1 was not significantly different (P = 0.757). This demonstrates a feeding preference associated with the overexpression genotype, not that MYB51 alone determines all insect resistance. MYB51 transcripts also rose within approximately 10 minutes after mechanical injury, peaked around 30 minutes and declined after an hour. (gigolashvili2007thetranscriptionfactor pages 9-10, gigolashvili2007thetranscriptionfactor pages 8-9)

Integration with immunity and other transcription factors

Under the bacterial flagellin elicitor flg22, MYB51 is strongly induced and is especially important for inducing CYP79B2/B3 and CYP83B1 and for accumulating indole glucosinolates. A 2016 study distinguished its principal action on I3M biosynthesis from the PEN2-dependent hydrolysis of modified glucosinolates and subsequent feedback affecting other indolic metabolites. During infection by Plectosphaerella cucumerina, combined MYB loss impaired indole-glucosinolate defense and the triple mutant showed pen2-like susceptibility, but pathogen-induced camalexin could remain intact: reduced indole glucosinolates should therefore not be equated with a constitutive inability to synthesize every tryptophan-derived phytoalexin. (frerigmann2016regulationofpathogentriggered pages 7-10, frerigmann2016regulationofpathogentriggered pages 10-13, frerigmann2016regulationofpathogentriggered pages 1-5)

The regulatory hierarchy becomes more context-dependent in effector-triggered immunity. MYB51 expression increased approximately 100-fold after the P. syringae avrRpm1 challenge in the reported seedling system. WRKY33 occupied and activated the MYB51 promoter; both factors contributed to CYP79B2/B3 expression, but their effects on CYP82C2 opposed one another—WRKY33 activating and MYB51 repressing it. This explains why MYB51’s contribution to camalexin and 4OH-ICN is conditional and partly mediated through shared precursor supply, rather than demonstrating that it is their sole master regulator. (barco2020hierarchicalanddynamic pages 2-4, barco2020hierarchicalanddynamic pages 10-12, barco2020hierarchicalanddynamic pages 7-10, barco2020hierarchicalanddynamic pages 6-7)

A second regulatory input connects hormone signaling to MYB51 activity: the brassinosteroid-responsive factor BES1 associated with MYB51 in co-immunoprecipitation and nuclear bimolecular-fluorescence-complementation experiments, and BES1 reduced MYB51-dependent CYP79B3 and UGT74B1 promoter-reporter activation. This provides a mechanistic example of growth–defense signaling constraining MYB51-driven indole-glucosinolate transcription; it does not show that MYB51 is itself a brassinosteroid receptor. (liao2020brassinosteroidsantagonizejasmonateactivated pages 19-25)

Recent research, applications and limits of inference

Recency and organism boundary. The strongest locus-specific functional experiments identified here date from 2007–2020. Relevant 2023–2024 publications frequently investigate other glucosinolate regulators or MYB51 orthologs, rather than adding comparable direct molecular evidence for Arabidopsis At1g18570. For example, a 2024 Arabidopsis light-signaling study experimentally implicated HY5–HDA9 repression at MYB29 and IMD1 promoters; it does not demonstrate HY5 binding the MYB51 promoter. Likewise, results for Brassica genes named BnaMYB51 or BoMYB51 must not be presented as experiments on O49782. This is a limit of the identified gene-specific literature, not evidence that the established MYB51 function has changed. (choi2024elongatedhypocotyl5 pages 1-1, gigolashvili2007thetranscriptionfactor pages 2-3, barco2020hierarchicalanddynamic pages 6-7)

Practical use remains chiefly research-stage. Arabidopsis MYB51 overexpression provides an experimentally demonstrated lever for increasing indole glucosinolates and altering herbivore feeding. As a translational example, a 2022 mapping study of 139 F₄ rocket (Eruca) lines identified 20 QTL and associated an Eruca MYB51 ortholog, among other candidates, with 4-methoxyglucobrassicin concentration. That is a candidate association for crop breeding, not functional validation of the Arabidopsis protein in rocket or evidence of a deployed MYB51-engineered cultivar. Context-dependent hormone inputs, regulator redundancy and MYB51-mediated repression of CYP82C2 also argue against assuming that simply increasing MYB51 will raise every desirable indolic defense product simultaneously. (gigolashvili2007thetranscriptionfactor pages 2-3, bell2022quantitativetraitloci pages 1-3, barco2020hierarchicalanddynamic pages 7-10, frerigmann2014myb34myb51and pages 3-4)

Key sources, with publication dates and URLs

References

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  2. (berger2007theroleofa pages 34-39): B Berger. The role of hig1/myb51 in the regulation of indolic glucosinolate biosynthesis. Unknown journal, 2007.

  3. (barco2020hierarchicalanddynamic pages 6-7): Brenden Barco and Nicole K. Clay. Hierarchical and dynamic regulation of defense-responsive specialized metabolism by wrky and myb transcription factors. Frontiers in Plant Science, Jan 2020. URL: https://doi.org/10.3389/fpls.2019.01775, doi:10.3389/fpls.2019.01775. This article has 48 citations.

  4. (frerigmann2014myb34myb51and pages 3-4): Henning Frerigmann and Tamara Gigolashvili. Myb34, myb51, and myb122 distinctly regulate indolic glucosinolate biosynthesis in arabidopsis thaliana. Molecular plant, 7 5:814-28, May 2014. URL: https://doi.org/10.1093/mp/ssu004, doi:10.1093/mp/ssu004. This article has 398 citations and is from a highest quality peer-reviewed journal.

  5. (barco2020hierarchicalanddynamic pages 2-4): Brenden Barco and Nicole K. Clay. Hierarchical and dynamic regulation of defense-responsive specialized metabolism by wrky and myb transcription factors. Frontiers in Plant Science, Jan 2020. URL: https://doi.org/10.3389/fpls.2019.01775, doi:10.3389/fpls.2019.01775. This article has 48 citations.

  6. (gigolashvili2007thetranscriptionfactor pages 3-5): Tamara Gigolashvili, Bettina Berger, Hans‐Peter Mock, Caroline Müller, Bernd Weisshaar, and Ulf‐Ingo Flügge. The transcription factor hig1/myb51 regulates indolic glucosinolate biosynthesis in arabidopsis thaliana. The Plant journal : for cell and molecular biology, 50 5:886-901, Apr 2007. URL: https://doi.org/10.1111/j.1365-313x.2007.03099.x, doi:10.1111/j.1365-313x.2007.03099.x. This article has 496 citations.

  7. (barco2020hierarchicalanddynamic media c75a5469): Brenden Barco and Nicole K. Clay. Hierarchical and dynamic regulation of defense-responsive specialized metabolism by wrky and myb transcription factors. Frontiers in Plant Science, Jan 2020. URL: https://doi.org/10.3389/fpls.2019.01775, doi:10.3389/fpls.2019.01775. This article has 48 citations.

  8. (barco2020hierarchicalanddynamic pages 7-10): Brenden Barco and Nicole K. Clay. Hierarchical and dynamic regulation of defense-responsive specialized metabolism by wrky and myb transcription factors. Frontiers in Plant Science, Jan 2020. URL: https://doi.org/10.3389/fpls.2019.01775, doi:10.3389/fpls.2019.01775. This article has 48 citations.

  9. (liao2020brassinosteroidsantagonizejasmonateactivated pages 19-25): Ke Liao, Yu-Jun Peng, Li-Bing Yuan, Yang-Shuo Dai, Qin-Fang Chen, Lu-Jun Yu, Ming-Yi Bai, Wen-Qing Zhang, Li-Juan Xie, and Shi Xiao. Brassinosteroids antagonize jasmonate-activated plant defense responses through bri1-ems-suppressor1 (bes1)1. Plant Physiology, 182:1066-1082, Nov 2020. URL: https://doi.org/10.1104/pp.19.01220, doi:10.1104/pp.19.01220. This article has 104 citations and is from a highest quality peer-reviewed journal.

  10. (gigolashvili2007thetranscriptionfactor pages 12-13): Tamara Gigolashvili, Bettina Berger, Hans‐Peter Mock, Caroline Müller, Bernd Weisshaar, and Ulf‐Ingo Flügge. The transcription factor hig1/myb51 regulates indolic glucosinolate biosynthesis in arabidopsis thaliana. The Plant journal : for cell and molecular biology, 50 5:886-901, Apr 2007. URL: https://doi.org/10.1111/j.1365-313x.2007.03099.x, doi:10.1111/j.1365-313x.2007.03099.x. This article has 496 citations.

  11. (frerigmann2014myb34myb51and pages 11-12): Henning Frerigmann and Tamara Gigolashvili. Myb34, myb51, and myb122 distinctly regulate indolic glucosinolate biosynthesis in arabidopsis thaliana. Molecular plant, 7 5:814-28, May 2014. URL: https://doi.org/10.1093/mp/ssu004, doi:10.1093/mp/ssu004. This article has 398 citations and is from a highest quality peer-reviewed journal.

  12. (gigolashvili2007thetranscriptionfactor pages 9-10): Tamara Gigolashvili, Bettina Berger, Hans‐Peter Mock, Caroline Müller, Bernd Weisshaar, and Ulf‐Ingo Flügge. The transcription factor hig1/myb51 regulates indolic glucosinolate biosynthesis in arabidopsis thaliana. The Plant journal : for cell and molecular biology, 50 5:886-901, Apr 2007. URL: https://doi.org/10.1111/j.1365-313x.2007.03099.x, doi:10.1111/j.1365-313x.2007.03099.x. This article has 496 citations.

  13. (gigolashvili2007thetranscriptionfactor pages 8-9): Tamara Gigolashvili, Bettina Berger, Hans‐Peter Mock, Caroline Müller, Bernd Weisshaar, and Ulf‐Ingo Flügge. The transcription factor hig1/myb51 regulates indolic glucosinolate biosynthesis in arabidopsis thaliana. The Plant journal : for cell and molecular biology, 50 5:886-901, Apr 2007. URL: https://doi.org/10.1111/j.1365-313x.2007.03099.x, doi:10.1111/j.1365-313x.2007.03099.x. This article has 496 citations.

  14. (frerigmann2016regulationofpathogentriggered pages 7-10): Henning Frerigmann, Mariola Piślewska-Bednarek, Andrea Sánchez-Vallet, Antonio Molina, Erich Glawischnig, Tamara Gigolashvili, and Paweł Bednarek. Regulation of pathogen-triggered tryptophan metabolism in arabidopsis thaliana by myb transcription factors and indole glucosinolate conversion products. Molecular plant, 9 5:682-695, May 2016. URL: https://doi.org/10.1016/j.molp.2016.01.006, doi:10.1016/j.molp.2016.01.006. This article has 182 citations and is from a highest quality peer-reviewed journal.

  15. (frerigmann2016regulationofpathogentriggered pages 10-13): Henning Frerigmann, Mariola Piślewska-Bednarek, Andrea Sánchez-Vallet, Antonio Molina, Erich Glawischnig, Tamara Gigolashvili, and Paweł Bednarek. Regulation of pathogen-triggered tryptophan metabolism in arabidopsis thaliana by myb transcription factors and indole glucosinolate conversion products. Molecular plant, 9 5:682-695, May 2016. URL: https://doi.org/10.1016/j.molp.2016.01.006, doi:10.1016/j.molp.2016.01.006. This article has 182 citations and is from a highest quality peer-reviewed journal.

  16. (frerigmann2016regulationofpathogentriggered pages 1-5): Henning Frerigmann, Mariola Piślewska-Bednarek, Andrea Sánchez-Vallet, Antonio Molina, Erich Glawischnig, Tamara Gigolashvili, and Paweł Bednarek. Regulation of pathogen-triggered tryptophan metabolism in arabidopsis thaliana by myb transcription factors and indole glucosinolate conversion products. Molecular plant, 9 5:682-695, May 2016. URL: https://doi.org/10.1016/j.molp.2016.01.006, doi:10.1016/j.molp.2016.01.006. This article has 182 citations and is from a highest quality peer-reviewed journal.

  17. (barco2020hierarchicalanddynamic pages 10-12): Brenden Barco and Nicole K. Clay. Hierarchical and dynamic regulation of defense-responsive specialized metabolism by wrky and myb transcription factors. Frontiers in Plant Science, Jan 2020. URL: https://doi.org/10.3389/fpls.2019.01775, doi:10.3389/fpls.2019.01775. This article has 48 citations.

  18. (choi2024elongatedhypocotyl5 pages 1-1): Dasom Choi, Seong-Hyeon Kim, Da-Min Choi, Heewon Moon, Jeong-Il Kim, Enamul Huq, and Dong-Hwan Kim. Elongated hypocotyl 5 interacts with histone deacetylase 9 to suppress glucosinolate biosynthesis in arabidopsis. Plant physiology, 196:1340-1355, May 2024. URL: https://doi.org/10.1093/plphys/kiae284, doi:10.1093/plphys/kiae284. This article has 22 citations and is from a highest quality peer-reviewed journal.

  19. (bell2022quantitativetraitloci pages 1-3): Luke Bell, Martin Chadwick, Manik Puranik, Richard Tudor, Lisa Methven, and Carol Wagstaff. Quantitative trait loci analysis of glucosinolate, sugar, and organic acid concentrations in eruca vesicaria subsp. sativa. Molecular Horticulture, Oct 2022. URL: https://doi.org/10.1186/s43897-022-00044-x, doi:10.1186/s43897-022-00044-x. This article has 6 citations.

Artifacts

Citations

  1. barco2020hierarchicalanddynamic pages 6-7
  2. barco2020hierarchicalanddynamic pages 7-10
  3. gigolashvili2007thetranscriptionfactor pages 2-3
  4. liao2020brassinosteroidsantagonizejasmonateactivated pages 19-25
  5. bell2022quantitativetraitloci pages 1-3
  6. berger2007theroleofa pages 34-39
  7. barco2020hierarchicalanddynamic pages 2-4
  8. gigolashvili2007thetranscriptionfactor pages 3-5
  9. gigolashvili2007thetranscriptionfactor pages 12-13
  10. gigolashvili2007thetranscriptionfactor pages 9-10
  11. gigolashvili2007thetranscriptionfactor pages 8-9
  12. frerigmann2016regulationofpathogentriggered pages 7-10
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  14. frerigmann2016regulationofpathogentriggered pages 1-5
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  17. Barco and Clay, 2020
  18. Liao et al., 2020
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