dcsimg

Taphrina deformans

provided by EOL authors
Taphrina deformans Taphrina deformans (Berk.) Tul (1866) is a causal organism of peach leaf curl disease. However the fungus is not limited only to peach (Prunus persica) and rather attacks the other Prunus species, almond (Prunus amygdalus) but to lesser extent (3). In US the annual loss is estimated to be 2.5 to 3 million dollars Contents Taxonomy The genus Taphrina was first described by Fries (1832) from poplar plant, where he isolated the fungus and named it Taphrina populina. Taphrina deformans was described by Tulasne in 1866. The first monograph of the genus Taphrina by Sadebeck (1893) distinguished 3 genera within the family Taphrinaceae namely: Exoascus, Magnusiella and Taphrina. Last monograph suggests that the order Taphrinales has only a single famlily Taphrinaceae with a single genus Taphrina but some workers describes the order Taphrinales has two family Protomyceateae with five genera and family Taphrinaceae with single genus Taphrina. Hierarchal classification of the fungus Domain: Eukaryota Kingdom: Fungi Subkingdom: Dikarya Phylum: Ascomycota Subphylum: Taphrinamycotina Class: Taphrinomycetes Order: Taphrinales Family: Taphrinaceae Genus: Taphrina Species: deformans Synonyms Ascomyces deformans Berk. Ascosporium deformans (Berk.) Berk. Taphrina deformans (Berk.) Tul. var. deformans Exoascus deformans (Berk.) Fuckel Exoascus deformans (Berk.) Fuckel var. deformans Ascomyces deformans Berk. var. deformans Exoascus deformans b cerasi Fuckel Taphrina deformans var. armeniaca Ikeno Exoascus deformans var. armeniaca (Ikeno) Sacc. & Traverso Exoascus amygdali Jacz. Taphrina amygdali (Jacz.) Mix Lalaria deformans R.T. Moore Genetics and phylogeny of the fungus The genome of Taphrina deformans has been recently sequenced and reveals a genome size of 13.3 Mega base pair (Mbp). The GC content is relatively high (49.5%). The fungus shares 83% similarity in terms of protein coding genes with other fungus. The virulence and host adaptation mechanisms are reflected in the genome. The fungus carries the genes for cell wall degradation which is essential for the process of infection; secondary metabolites necessary for colonization; phytohormones and carotenoids for the symptom development. The virulence of the fungus is primarily associated with lipid metabolizing genes. Different species of the fungus Taphrina are host specific. The phylogenetic analysis reveals the specific symptom associated with distinct species. Before the development of the molecular markers people were able to identify Taphrina species based on their morphology, host, and infection type. Now the advancement in the molecular tools supports the earlier concept of species identification, this is because the Taphrina species are genetically distinct. Morphology The fungus is highly characterized by its dimorphic growth stages. The unicellular yeast stage is saprophytic in nature whereas the filamentous stage is the pathogenic stage. Only the yeast stage can be grown the culture media. The mycelium is septate, intercellular in nature, hyline and branched and present only in reddened diseased area of the leaf. The identifying character of this fungus is that they donot form the ascocarp. The asci are naked (no ascocarp formation) and is usually developed on the upper surface of the leaf. The shape of ascus is cylindrical and rounded at the apex measuring 32-39*12-14 µm. Typically eight ascospores are formed within the ascus. Ascospores are spherical or ovoid in shape and measures 3-7 µm in diameter. The ascus wall at the apex ruptures causing the ascospores release in the atmosphere. Budding in common in ascospore resulting in numerous blastospores. Blastospores continue the budding process even after release. Ecology The fungus is cosmopolitan in nature and has been detected from different peach growing countries (New Zealand, Australia, India, and Russia). The fungus is mostly reported from the temperate region of the world. Taphrina deformans as plant pathogen. Symptoms The symptoms of the disease are prominent in the early spring. The disease starts with small yellowish or reddish area at the site of infection. The symptoms of the fungus infection and development are readily visible in leaves nonetheless the fungus also affects blossoms, twigs and fruits. Infected leaves become distorted and curled. The curling is usually downwards. Reddening of the infected leaf is a typical symptom which is associated with production of plant hormone indole-3-acetic-acid (IAA) (17). Fruit infection is not so common but cracking of the fruit, corky surface and premature fruit drop may be observed occasionally. The pathogen itself does not kill the tree but the losses are due to decrease in the yield. Disease cycle and epidemiology Earlier worker Sadebeck (1893) believed that the mycelium of the fungus would survive in the twigs and is responsible for the disease next year. But Pierce (1900) was not in agreement with the concept of mycelial survival in the twigs. Some workers believed the survival was through the ascospores. The disease cycle starts when the overwintering bud conidia/ blastospores/ yeast cells come in contact with the young leaves. These structures overwinter in the bark and bud scales of the tree and acts as the primary source of inoculums. Under favorable climatic conditions these structures germinate to produce short hyphae which grow intercellular. Cool and rainy weather is conducive for germination and infection process. Generally the juvenile tissue of the plant is more susceptible to the disease. The incubation period ranges from 9-33 days. Immediately after the symptom development the fungus produces the sac like structure called asci. The ascus development takes place at night. Usually 8 sexual spores called ascospores are borne in these asci. The rupturing of the ascus wall causes release of spores into other healthy tissue. The spores are carried away by wind and water splash. The ascospores continue budding in and out of ascus. The fungus survives harsh environment in the form of ascospores and bud conidia which acts as a reservoir of inoculums for the next season. The disease is favored by the cool and moist weather. The disease incidence and severity is dependent on many factors namely rainfall, wetness duration and incubation temperature. Wetness is more important than the rainfall(14). The minimum rainfall of 3mm with the wetness duration of at least 12.5 hour is sufficient for infection. The infection probability is maximum at 24° C and a wet period of 2 days. Temperatures ranging from 12-16° C are favorable for budding and germ tube formation. The optimum temperature for fungal growth in lab is around 20° C. Budding is favored by the high relative humidity (95%). Management The disease is difficult to manage once the infection has occurred. Till date no peach cultivar is completely resistant to the disease. However some varieties like Muir, Q-18, Frost and Indian Free are resistant to some extent. Removal of the diseased leaves won’t help much because the pathogen survives in bark and bud scales. Therefore the management of the disease heavily relies on the fungicide application. The timing of fungicide application is crucial in disease management. The disease can be controlled by the application of one of the fungicides (carbendazim, captafol thiram ziram captan chorothalinol) one after the fall in autumn and other before the buds start to swell in the spring. Some workers suggests maintaining the tree vigor via fertilization, frequent irrigation and thinning of fruit can be effective in disease management.
license
cc-by-3.0
copyright
Shankar Shakya
partner site
EOL authors

Taphrina deformans

provided by wikipedia EN

Taphrina deformans is a fungus and plant pathogen, and a causal agent[s] of peach leaf curl.[1]

Taphrina Deformans

Life cycle

Taphrina deformans infects species of the genus Prunus (including P. amygdalus (almond) and P. persica (peach)).[2] It has been observed that this fungus also infects the fruits of some South American trees like Ocotea puberula, Nectandra megapotamica and other Lauraceae species. Infected leaves develop a whitish bloom as the infection progresses. This bloom consists of asci that break through the cuticle of the leaf by way of lysis.[3] One ascus contains eight ascospores that create conidia, which are ejected in early summer and moved by rain and wind. This fungus is believed to survive the winter by staying on the surface of the new host plant, such as on bark or buds.[4] In the spring, new buds are infected by the conidia as the leaves emerge from the buds. The disease does not occur every year, as it requires a minimum of 3mm of rainfall followed by at least 12 days during which the developing conidia remain damp and at temperatures below 19 °C.[5][6] The fungus has higher infection rates following cooler, damper winters.[6]

Taphrina deformans hyphae growing in intercellular spaces secrete polysaccharide-degrading enzymes, such as cellulase, causing partial dissolution of the host cell wall. This process also results in changes in the plasma membrane.[3] T. deformans also produces the auxin indole-3-acetic acid from L-tryptophan via indole-3-pyruvic acid and indole-3-acetaldehyde. This process is thought to be responsible for the hyperplastic effect of the infection.[7]

Taphrina deformans genome

Taphrina deformans genome has been sequenced.[8] The genome carries characteristic genes that are important for the plant infection process.

References

  1. ^ Peach leaf curl, Taphrina deformans Archived 2007-08-29 at the Wayback Machine. at West Virginia University
  2. ^ Mix AJ. (1956). “Notes on Some Species of Taphrina”. Transactions of the Kansas Academy of Science 59 (4): 465-482
  3. ^ a b Bassi M, Conti GG, & Barbieri N. (1984). “Cell wall degradation by Taphrina deformans in host leaf cells.” Mycopathologia 88 (2-3) 115–125
  4. ^ Gray, William D.. The Relation of Fungi to Human Affairs. New York: Henry Holt and Company, Inc., 1959. Print.
  5. ^ Rossi V, Bolognesi M, Languasco L, & Giosuè S. (2006). “Influence of Environmental Conditions on Infection of Peach Shoots by Taphrina deformansEcology and Epidemiology 96 (2) 155-163
  6. ^ a b Smith, S.E. What is Peach Leaf Curl? 2009. WiseGEEK. 14 Apr 2009 <http://www.wisegeek.com/what-is-peach-leaf-curl.htm>
  7. ^ Yamada Y, Tsukamoto H, Shiraishi T, Nomura T, & Oku H. (1990). “Detection of Indoleacetic Acid Biosynthesis in Some Species of Taphrina Causing Hyperplastic Diseases in Plants” Annals of the Phytopathological Society of Japan. 56 532–540
  8. ^ Cisse, O. H., J. M. Almeida, A. Fonseca, A. A. Kumar, J. Salojarvi, K. Overmyer, P. M. Hauser and M. Pagni (2013). “Genome sequencing of the plant pathogen Taphrina deformans, the causal agent of peach leaf curl." MBio 4(3) e00055-00013.

license
cc-by-sa-3.0
copyright
Wikipedia authors and editors
original
visit source
partner site
wikipedia EN

Taphrina deformans: Brief Summary

provided by wikipedia EN

Taphrina deformans is a fungus and plant pathogen, and a causal agent[s] of peach leaf curl.

Taphrina Deformans
license
cc-by-sa-3.0
copyright
Wikipedia authors and editors
original
visit source
partner site
wikipedia EN