Indole-3-acetic acid

Indole-3-acetic acid
Names
IUPAC name
2-(1H-indol-3-yl)acetic acid
Systematic IUPAC name
2-(1H-indol-3-yl)ethanoic acid
Other names
Indole-3-acetic acid,
indolylacetic acid,
1H-Indole-3-acetic acid,
indoleacetic acid,
heteroauxin,
IAA
Identifiers
87-51-4 YesY
3D model (Jmol) Interactive image
ChEBI CHEBI:16411 YesY
ChEMBL ChEMBL82411 YesY
ChemSpider 780 YesY
DrugBank DB07950 YesY
ECHA InfoCard 100.001.590
KEGG C00954 YesY
PubChem 802
Properties
C10H9NO2
Molar mass 175.19 g·mol−1
Appearance White solid
Melting point 168 to 170 °C (334 to 338 °F; 441 to 443 K)
Moderate
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
YesY verify (what is YesYN ?)
Infobox references

Indole-3-acetic acid (IAA, 3-IAA) is the most common, naturally-occurring, plant hormone of the auxin class. It is the best known of the auxins, and has been the subject of extensive studies by plant physiologists.[1] IAA is a derivative of indole, containing a carboxymethyl substituent. It is a colorless solid that is soluble in polar organic solvents.

Biosynthesis

Main article: Auxin

IAA is predominantly produced in cells of the apex (bud) and very young leaves of a plant. Plants can synthesize IAA by several independent biosynthetic pathways. Four of them start from tryptophan, but there is also a biosynthetic pathway independent of tryptophan.[2] Plants mainly produce IAA from tryptophan through indole-3-pyruvic acid.[3][4] IAA is also produced from tryptophan through indole-3-acetaldoxime in Arabidopsis thaliana.[5]

In rats, IAA is a product of both endogenous and colonic microbial metabolism from dietary tryptophan along with tryptophol. This was first observed in rats infected by Trypanosoma brucei gambiense.[6] and correlation with protein intake has been confirmed in 2015. Humans did not excrete IAA.[7]

Biological effects

As all auxins, IAA has many different effects, such as inducing cell elongation and cell division with all subsequent results for plant growth and development. On a larger scale, IAA serves as signaling molecule necessary for development of plant organs and coordination of growth.

Plant gene regulation

IAA enters the plant cell nucleus and binds to a protein complex composed of a ubiquitin-activating enzyme (E1), a ubiquitin-conjugating enzyme (E2), and a ubiquitin ligase (E3), resulting in ubiquitination of Aux/IAA proteins with increased speed.[8] Aux/IAA proteins bind to auxin response factor (ARF) proteins, forming a heterodimer, suppressing ARF activity.[9] In 1997 it was described how ARF's bind to auxin-response gene elements in promoters of auxin regulated genes, generally activating transcription of that gene when an Aux/IAA protein is not bound.[10]

IAA inhibits the photorespiratory-dependent cell death in photorespiratory catalase mutants. This suggests a role for auxin signalling in stress tolerance.[11]

Bacterial physiology

IAA production is widespread among environmental bacteria that inhabit soils, waters, but also plant and animal hosts. Distribution and substrate specificity of the involved enzymes suggests these pathways play a role beyond plant-microbe interactions.[12] Enterobacter cloacae can produce IAA, from aromatic and branched-chain amino acids.[13]

Fungal symbiosis

Fungi can form a fungal mantle around roots of perennial plants called ectomycorrhiza. a fungus specific to spruce called Tricholoma vaccinum was shown to produce IAA from tryptophan and excrete it from its hyphae. This induced branching in cultures, and enhanced Hartig net formation. The fungus uses a multidrug and toxic extrusion (MATE) transporter Mte1.[14] Research into IAA-producing fungi to promote plant growth and protection in sustainable agriculture is underway.[15]

Synthesis

Chemically, it can be synthesized by the reaction of indole with glycolic acid in the presence of base at 250 °C:[16]

Alternatively the compound has been synthesized by Fischer indole synthesis using Glutamic acid and Phenylhydrazine.[17] Glutamic acid was converted to the necessary aldehyde via Strecker degradation.

Many methods for its synthesis have been developed since its original synthesis from indole-3-acetonitrile.[18]

History and synthetic analogs

William Gladstone Tempelman studied substances for growth promotion at Imperial Chemical Industries Ltd. After 7 years of research he changed the direction of his study to try the same substances at high concentrations in order to stop plant growth. In 1940 he published his finding that IAA killed broadleaf plants within a cereal field.[19]

The search for an acid with a longer half life, i.e. a metabolically and environmentally more stable compound led to 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), both phenoxy herbicides and analogs of IAA. Robert Pokorny an industrial chemist for the C.B. Dolge Company in Westport, Connecticut published their synthesis in 1941.[20]

Other less expensive synthetic auxin analogs on the market for use in horticulture are indole-3-butyric acid (IBA) and 1-naphthaleneacetic acid (NAA). When sprayed on broad-leaf dicot plants, they induce rapid, uncontrolled growth, eventually killing them. First introduced in 1946, these herbicides were in widespread use in agriculture by the middle of the 1950s.

Mammalian toxicity/ health effects

Little research has been conducted on the effects of IAA on humans and toxicity data are limited. No data on human carcinogenic, teratogenic, or developmental effects have been created.

IAA is listed in its MSDS as mutagenic to mammalian somatic cells, and possibly carcinogenic based on animal data. It may cause adverse reproductive effects (fetotoxicity) and birth defects based on animal data. No human data as of 2008. It is listed as a potential skin, eye, and respiratory irritant, and users are warned not to ingest it. Protocols for ingestion, inhalation, and skin/eye exposure are standard for moderately poisonous compounds and include thorough rinsing in the case of skin and eyes, fresh air in the case of inhalation, and immediately contacting a physician in all cases to determine the best course of action and not to induce vomiting when of ingested. The NFPA 704 health hazard rating for IAA is 2, which denotes a risk of temporary incapacitation with intense or prolonged, but not chronic exposure, and a possibility of residual injury.[21]

Developmental toxicity

IAA produces microcephaly in rats during the early stage of cerebral cortex development. IAA decreased the locomotor activities of rat embryos/fetuses; treatment with IAA and analog 1(methyl)-IAA resulted in apoptosis of neuroepithelial cell and significantly decreased brain sizes relative to body weight in embryonic rats.[22]

Immunotoxin

IAA is an apoptosis-inducing ligand in mammals. As of 2010, the signal transduction pathways are as follows: IAA/HRP activates p38 mitogen-activated protein kinases and c-Jun N-terminal kinases. It induces caspase-8 and caspase-9, which results in caspase-3 activation and poly(adp-ribose) polymerases cleavage.[23]

In 2002 it had been hypothesized that IAA coupled with horseradish peroxidase (HRP) could be used in targeted cancer therapy. Radical-IAA molecules would attach to cells marked by HRP and HRP reactive cells would be selectively killed.[24] In 2010 in vitro experiments proved this concept of IAA as an immunotoxin when used in preclinical studies of targeted cancer therapy, as it induced apoptosis in bladder[23] and in hematological malignancies.[25]

References

  1. ↑ Simon, Sibu; Petrášek, Jan (2011). "Why plants need more than one type of auxin". Plant Science. 180 (3): 454–60. doi:10.1016/j.plantsci.2010.12.007. PMID 21421392.
  2. ↑ Zhao, Yunde (2010). "Auxin Biosynthesis and Its Role in Plant Development". Annual Review of Plant Biology. 61: 49–64. doi:10.1146/annurev-arplant-042809-112308. PMC 3070418Freely accessible. PMID 20192736.
  3. ↑ Mashiguchi, Kiyoshi; Tanaka, Keita; Sakai, Tatsuya; Sugawara, Satoko; Kawaide, Hiroshi; Natsume, Masahiro; Hanada, Atsushi; Yaeno, Takashi; et al. (2011). "The main auxin biosynthesis pathway in Arabidopsis". Proceedings of the National Academy of Sciences. 108 (45): 18512–7. Bibcode:2011PNAS..10818512M. doi:10.1073/pnas.1108434108. PMC 3215075Freely accessible. PMID 22025724.
  4. ↑ Won, Christina; Shen, Xiangling; Mashiguchi, Kiyoshi; Zheng, Zuyu; Dai, Xinhua; Cheng, Youfa; Kasahara, Hiroyuki; Kamiya, Yuji; et al. (2011). "Conversion of tryptophan to indole-3-acetic acid by TRYPTOPHAN AMINOTRANSFERASES OF ARABIDOPSIS and YUCCAs in Arabidopsis". Proceedings of the National Academy of Sciences. 108 (45): 18518–23. Bibcode:2011PNAS..10818518W. doi:10.1073/pnas.1108436108. PMC 3215067Freely accessible. PMID 22025721.
  5. ↑ Sugawara, Satoko; Hishiyama, Shojiro; Jikumaru, Yusuke; Hanada, Atsushi; Nishimura, Takeshi; Koshiba, Tomokazu; Zhao, Yunde; Kamiya, Yuji; Kasahara, Hiroyuki (2009). "Biochemical analyses of indole-3-acetaldoxime-dependent auxin biosynthesis in Arabidopsis". Proceedings of the National Academy of Sciences. 106 (13): 5430–5. Bibcode:2009PNAS..106.5430S. doi:10.1073/pnas.0811226106. JSTOR 40455212. PMC 2664063Freely accessible. PMID 19279202.
  6. ↑ Howard Stibbs Henry; Richard Seed John (1975). "Short-Term Metabolism of [14C]Tryptophan in Rats Infected with Trypanosoma brucei gambiense". J Infect Dis. 131 (4): 459–462. doi:10.1093/infdis/131.4.459. PMID 1117200.
  7. ↑ Poesen R, Mutsaers HA, et al. (Oct 2015). "The Influence of Dietary Protein Intake on Mammalian Tryptophan and Phenolic Metabolites". PLOS ONE. 10 (10): e0140820. doi:10.1371/journal.pone.0140820.
  8. ↑ Pekker, MD; Deshaies, RJ (2005). "Function and regulation of cullin-RING ubiquitin ligases.". Plant Cell. (6): 9–20.
  9. ↑ Tiwari, SB; Hagen, G; Guilfoyle, TJ (2004). "Aux/IAA proteins contain a potent transcriptional repression domain.". Plant Cell. 16: 533–43. doi:10.1105/tpc.017384.
  10. ↑ Ulmasov, T; Hagen, G; Guilfoyle, TJ (1997). "ARF1, a transcription factor that binds to auxin response elements.". Science. 276: 1865–68. doi:10.1126/science.276.5320.1865. PMID 9188533.
  11. ↑ Kerchev P, Muhlenbock P, Denecker J, Morreel K, Hoeberichts FA, van der Kelen K, Vandorpe M, Nguyen L, Audenaert D, van Breusegem F (Feb 2015). "Activation of auxin signalling counteracts photorespiratory H2O2-dependent cell death". Plant Cell Environ. 38 (2): 253–65. doi:10.1111/pce.12250. PMID 26317137.
  12. ↑ Patten CL, Blakney AJ, Coulson TJ (Nov 2013). "Activity, distribution and function of indole-3-acetic acid biosynthetic pathways in bacteria". Crit Rev Microbiol. 39 (4): 395–415. doi:10.3109/1040841X.2012.716819.
  13. ↑ Parsons CV, Harris DM, Patten CL, et al. (Sep 2015). "Regulation of indole-3-acetic acid biosynthesis by branched-chain amino acids in Enterobacter cloacae UW5". FEMS Microbiol Lett. 362 (18): fnv153. doi:10.1093/femsle/fnv153.
  14. ↑ Krause K, Henke C, Asiimwe T, Ulbricht A, Klemmer S, Schachtschabel D, Boland W, Kothe E (Oct 2015). "Biosynthesis and Secretion of Indole-3-Acetic Acid and Its Morphological Effects on Tricholoma vaccinum-Spruce Ectomycorrhiza". Appl Environ Microbiol. 81 (20): 7003–11. doi:10.1128/AEM.01991-15.
  15. ↑ Fu SF1 Wei JY, Chen HW, Liu YY, Lu HY, Chou JY (Aug 2015). "Indole-3-acetic acid: A widespread physiological code in interactions of fungi with other organisms". Plant Signal Behav. 10 (8): e1048052. doi:10.1080/15592324.2015.1048052.
  16. ↑ Johnson, Herbert E.; Crosby, Donald G. (1964). "Indole-3-acetic Acid". Org. Synth. 44: 64.; Coll. Vol., 5, p. 654
  17. ↑ Fox, Sidney W.; Bullock, Milon W. (1951). "Synthesis of Indoleacetic Acid from Glutamic Acid and a Proposed Mechanism for the Conversion". Journal of the American Chemical Society. 73 (6): 2754–2755. doi:10.1021/ja01150a094.
  18. ↑ Majima, Rikō; Hoshino, Toshio (1925). "Synthetische Versuche in der Indol-Gruppe, VI.: Eine neue Synthese von β-Indolyl-alkylaminen". Berichte der deutschen chemischen Gesellschaft (A and B Series). 58 (9): 2042–6. doi:10.1002/cber.19250580917.
  19. ↑ Templeman W. G.; Marmoy C. J. (2008). "The effect upon the growth of plants of watering with solutions of plant-growth substances and of seed dressings containing these materials". Annals of Applied Biology. 27 (4): 453–471. doi:10.1111/j.1744-7348.1940.
  20. ↑ Pokorny Robert (1941). "New Compounds. Some Chlorophenoxyacetic Acids". J. Am. Chem. Soc. 63 (6): 1768–1768. doi:10.1021/ja01851a601.
  21. ↑ "Indole-3-Acetic Acid: Material Safety Data Sheet." November 2008.
  22. ↑ Furukawa, Satoshi; Usuda, Koji; Abe, Masayoshi; Ogawa, Izumi (2005). "Effect of Indole-3-Acetic Acid Derivatives on Neuroepithelium in Rat Embryos". The Journal of Toxicological Sciences. 30 (3): 165–74. doi:10.2131/jts.30.165. PMID 16141651.
  23. 1 2 Jeong YM1, Oh MH, Kim SY, Li H, Yun HY, Baek KJ, Kwon NS, Kim WY, Kim DS. Indole-3-acetic acid/horseradish peroxidase induces apoptosis in TCCSUP human urinary bladder carcinoma cells.Pharmazie. 2010, Feb;65(2):122-6.PMID 20225657
  24. ↑ Wardman P. Indole-3-acetic acids and horseradish peroxidase: a new prodrug/enzyme combination for targeted cancer therapy. Curr Pharm Des. 2002;8(15):1363-74. Review. PMID 12052213
  25. ↑ Dalmazzo LF, Santana-Lemos BA, Jácomo RH, Garcia AB, Rego EM, da Fonseca LM, Falcão RP. Antibody-targeted horseradish peroxidase associated with indole-3-acetic acid induces apoptosis in vitro in hematological malignancies.Leuk Res. 2011 May;35(5):657-62. doi: 10.1016/j.leukres.2010.11.025. PMID 21168913 cited in: Alan S. Wayne et al. Immunotoxins for leukemia. Blood. 2014 Apr 17; 123(16): 2470–2477. doi: 10.1182/blood-2014-01-492256 PMCID: PMC3990911. review
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