Fungicide

Source: Wikipedia, the free encyclopedia.

Fungicides are

oomycetes, which are not taxonomically/genetically fungi, although sharing similar methods of infecting plants. Fungicides can either be contact, translaminar or systemic. Contact fungicides are not taken up into the plant tissue and protect only the plant where the spray is deposited. Translaminar fungicides redistribute the fungicide from the upper, sprayed leaf surface to the lower, unsprayed surface. Systemic fungicides are taken up and redistributed through the xylem vessels. Few fungicides move to all parts of a plant. Some are locally systemic, and some move upward.[2][3]
Most fungicides that can be bought retail are sold in liquid form, the active ingredient being present at 0.08% in weaker concentrates, and as high as 0.5% for more potent fungicides. Fungicides in powdered form are usually around 90% sulfur.

Safety

Fungicide

Ziram is also a fungicide that is toxic to humans with long-term exposure, and fatal if ingested.[6]
A number of fungicides are also used in human health care.

Types of fungicides

Further information: List of fungicides

Like other pesticides, fungicides are numerous and diverse. This complexity has led to diverse schemes for classifying fungicides. Classifications are based on

inorganic vs organic, chemical structures, and, most successfully, mechanism of action (MOA). These respective classifications reflect the evolution of the underlying science
.

Traditional

Traditional fungicides are simple inorganic compounds like sulfur,[7] and copper salts. While cheap, they must be applied repeatedly and are relatively ineffective.[1] Other active ingredients in fungicides include neem oil, rosemary oil, jojoba oil, the bacterium Bacillus subtilis, and the beneficial fungus Ulocladium oudemansii.

Nonspecific

In the 1930s

ziram, zineb, maneb, and mancozeb. These compounds are non-specific and are thought to inhibit cysteine-based protease enzymes. Similarly nonspecific are N-substituted phthalimides. Members include captafol, captan, and folpet. Chlorothalonil is also non-specific.[1]

Specific

Specific fungicides target a particular biological process in the fungus.

Nucleic acid metabolism

Cytoskeleton and motor proteins

Respiration

Some fungicides target succinic dehydrogenase, a metabolically central enzyme. Fungi of the class Basidiomycetes were the initial focus of these fungicides. These fungi are active against cereals.

Amino acid and protein synthesis

Signal transduction

Lipid synthesis / membrane integrity

Melanin synthesis in cell wall

Sterol biosynthesis in membranes

Cell wall biosynthesis

Host plant defence induction

Mycoviruses

Some of the most common

biocontrols/biofungicides.[9]

Resistance

See also: Antimicrobial resistance

Doses that provide the most control of the disease also provide the largest selection pressure to acquire resistance.[10]

In some cases, the pathogen evolves resistance to multiple fungicides, a phenomenon known as

cross resistance. These additional fungicides typically belong to the same chemical family, act in the same way, or have a similar mechanism for detoxification. Sometimes negative cross-resistance occurs, where resistance to one chemical class of fungicides increases sensitivity to a different chemical class of fungicides. This has been seen with carbendazim and diethofencarb. Also possible is resistance to two chemically different fungicides by separate mutation events. For example, Botrytis cinerea is resistant to both azoles and dicarboximide fungicides
.

A common mechanism for acquiring resistance is alteration of the target enzyme. For example,

Black Sigatoka, an economically important pathogen of banana, is resistant to the QoI fungicides, due to a single nucleotide change resulting in the replacement of one amino acid (glycine) by another (alanine) in the target protein of the QoI fungicides, cytochrome b.[11] It is presumed that this disrupts the binding of the fungicide to the protein, rendering the fungicide ineffective. Upregulation of target genes can also render the fungicide ineffective. This is seen in DMI-resistant strains of Venturia inaequalis.[12]

Resistance to fungicides can also be developed by efficient

substrate specificities that together work to pump toxic chemicals out of the cell.[13]

In addition to the mechanisms outlined above, fungi may also develop metabolic pathways that circumvent the target protein, or acquire enzymes that enable the metabolism of the fungicide to a harmless substance.

Fungicides that are at risk of losing their potency due to resistance include Strobilurins such as azoxystrobin.[14] Cross-resistance can occur because the active ingredients share a common mode of action.[15] FRAC is organized by CropLife International.[16][14]

See also

Further reading

  • Haverkate, F.; Tempel, A.; Held, A. J. (1969). "Interaction of 2,4,5-trichlorophenylsulphonylmethyl thiocyanate with fungal spores". Netherlands Journal of Plant Pathology. 75 (5): 308–315.
    S2CID 23304303
    .

References

  1. ^
    ISBN 978-0-471-48494-3
    .
  2. ^ Mueller, Daren. "Fungicides:Terminology". Iowa State University. Retrieved June 1, 2013.
  3. S2CID 22200121
    .
  4. ^ Pesticide Chemistry and Bioscience edited by G.T Brooks and T.R Roberts. 1999. Published by the Royal Society of Chemistry
  5. ^ Hrelia et al. 1996 - The genetic and non-genetic toxicity of the fungicide Vinclozolin. Mutagenesis Volume 11 445-453
  6. ^ National Center for Biotechnology Information. PubChem Compound Database; CID=8722, https://pubchem.ncbi.nlm.nih.gov/compound/8722 (accessed Jan. 13, 2019)
  7. ^ C.Michael Hogan. 2011. Sulfur. Encyclopedia of Earth, eds. A.Jorgensen and C.J.Cleveland, National Council for Science and the environment, Washington DC Archived October 28, 2012, at the Wayback Machine
  8. doi:10.1111/j.1747-0765.2009.00365.x
    .
  9. S2CID 34331588
    .
  10. ^ Metcalfe, R.J. et al. (2000) The effect of dose and mobility on the strength of selection for DMI (sterol demethylation inhibitors) fungicide resistance in inoculated field experiments. Plant Pathology 49: 546–557
  11. ^ Sierotzki, Helge (2000) Mode of resistance to respiration inhibitors at the cytochrome bc1 enzyme complex of Mycosphaerella fijiensis field isolates Pest Management Science 56:833–841
  12. ^ Schnabel, G., and Jones, A. L. 2001. The 14a-demethylase (CYP51A1) gene is overexpressed in V. inaequalis strains resistant to myclobutanil. Phytopathology 91:102–110.
  13. ^ Zwiers, L. H. et al. (2003) ABC transporters of the wheat pathogen Mycosphaerella graminicola function as protectants against biotic and xenobiotic toxic compounds. Molecular Genetics and Genomics 269:499–507
  14. ^ a b "Fungicides Resistance Action Committee website".
  15. ^ "Fungal control agents sorted by cross resistance pattern and mode of action" (PDF). 2020. Archived from the original (PDF) on 2021-08-16. Retrieved 2020-09-04.
  16. ^ "Resistance Management". CropLife International. 2018-02-28. Retrieved 2020-11-22.

External links

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