Plasmopara halstedii

Plasmopara halstedii
Scientific classification
Domain: Eukaryota
(unranked): SAR
Superphylum: Heterokonta
Class: Oomycetes
Subclass: Incertae sedis
Order: Peronosporales
Family: Peronosporaceae
Genus: Plasmopara
Species: P. halstedii
Binomial name
Plasmopara halstedii
(Farl.) Berl. & De Toni, (1888)
Synonyms

Peronospora halstedii Farl., (1882)
Plasmopara helianthi Novot., (1962)

Plasmopara halstedii is a plant pathogen infecting sunflowers. The species is one of many pathogens commonly referred to as downy mildew.[1] P. halstedii originated in North America.

P. halstedii oospores produce a thin wall which are resistant structures, sexually produced that are essential for its continuation. After entering an area, the eradication of the pathogen is difficult due to the formation of oospores, which can remain viable in soil for many years.[2]

Hosts and Symptoms

Plasmopara halstedii is an obligate biotroph that attacks the flowering plants of the Asteraceae family, found to infect the genus’ Helianthus, Bidens, Artemisia, and Xanthium. The pathogen has the strongest impact on Helianthus, degrading flower yields in the species H. argophyllus, H. debilis, H. petiolaris and H. annuus.[3] H. annus, the common sunflower, is also the most common host of P. halstedii. Xanthium strumarium,[4] the common cocklebur, and Ambrosia artemisiifolia,[5] or ragweed, have been shown to act as significant wild hosts.

P. halstedii causes significant yield losses due to the production of infertile sunflowers. Infertility due to P. halstedii is a result of sporulation on the flowering bodies as well as seed damping off due to root infection.[3][6] Other symptoms include plant stunting, chlorosis, root browning and alteration of secondary metabolism of infected plants.[7]

As an oomycete, P. halstedii releases motile zoospores as secondary inoculum. In these cases, secondary infection symptoms are much less severe than primary symptoms.[8] A sign of the disease is the “typical downy appearance” resulting from sporulation the plant surface.[8]

Detection

Systemically infected sunflower plants may have some degree of stunting and the leaves show pale green or chlorotic mottling which spreads along the main veins and over the lamella.

Disease Cycle

P. halstedii is a plant pathogenic oomycete, capable of overwintering in soil due to survival structures called oospores. For this reason, P. halstedii is a soil borne pathogen infecting the roots of the host plant.[9] Oospores have the potential to live in soil up to 8 years,[6] while oospore germination takes 10–30 days.[10] Germination length depends on environmental condition and typically occurs in the spring. The germinating oospores form sporangia that release motile zoospores as a secondary inoculum.[10]

After primary infection, zoospores serve as a main source of inoculum throughout the rest of the season.[11] Zoospores germinate in about two hours and have two means of infection: direct penetration of the root through the use of an appresorium or infection due to an already present wound. Hyphae extend throughout the intercellular space, forming parasitic haustoria. The pathogen breaks through the surface of leaves and flowering structures through stomata. Asexual reproduction structures, called zoosporangiaphores, form at these sites. These structures release zoosporangia containing zoospores to other plants, the primary means of dissemination.[3]

Sexual reproduction be either homothallic or heterothallic. Homothallic reproduction is characterized by the fusion of the asexual oogonium and antheridium. This fusion leads to the formation and release of oospores, the primary inoculum for the next season. Heterothallic sexual reproduction is the fusion of sexual cells from two separate organisms, leading to "outcrossing".[10][12]

Management and Control

Once the pathogen has been detected in an area, management is essential, as P. halstedii is nearly impossible to eradicate. Between long surviving resting spores and high levels of secondary inoculum, P. halstedii can infect anywhere from 50% to 95% of sunflower yields in a single season.[6]

Resistant sunflower strains are available, as two types of dominant major resistance genes have been identified, denoted as Pl.[3] Type 1 resistance lacks infection above the base of the hypocotyl. Type 2 is characterized by a weak infection, with sporulation never reaching the upper region of the host.[3] Resistant genes have been overcome in the past as the pathogen evolves and mutates, suggesting that resistance may not give the best results.[13] However, due to the constant search for resistant sources from wild Helianthus, the gene pool of cultivars is frequently being used to produce new, commercially resistant strains.[14][15]

Seed treatment has been shown to be effective in controlling the disease, as the establishment of P. halstedii in an area of soil is nearly irreversible. The compounds metalaxyl and oxadixyl have been shown to protect seeds in the case of infection, and treatments containing these compounds are commercially available.[16] Fungicides seed dressings of this nature have also been shown to give significant control over the pathogen.[17] However, some strains of P. halstedii have begun to show resistance to metalaxyl-based fungicides, reported in multiple countries.[13][18] Alternate forms of resistance are being developed for the future, including the use of biological antagonists[14] and defense-related proteins.[19]

Australia is the leader in pest control of P. halstedii. In Australia, any imported seed is subject to hot-water treatment, fungicide dusting and monitoring for up to 3 years.[20]

References

  1. Friskop, Andrew; Markell, Sam; Gulya, Tom (2009). "Downy Mildew of Sunflower" (PDF). Sunflower Publications. IPM Publications. Fargo, North Dakota: North Dakota State University Extension Service. Retrieved 4 March 2016.
  2. Maria Villas Bôas de Campos Leite, Regina; Assis Henning, Ademir; Rosa Rodrigues, Silvia; Fernandes de Oliveira, Marcelo (December 2007). "Detecção e variabilidade de Plasmopara halstedii no Brasil e avaliação da resistência de genótipos de girassol ao míldio" [Detection and variability of Plasmopara halstedii in Brazil and resistance of sunflower genotypes to downy mildew]. Summa Phytopathologica. ISSN 0100-5405.
  3. 1 2 3 4 5 Gascuel, Q., Martinez, Y., Boniface, M.-C., Vear, F., Pichon, M. and Godiard, L. (2015), The sunflower downy mildew pathogen Plasmopara halstedii. Molecular Plant Pathology, 16: 109–122. doi:10.1111/mpp.12164
  4. Komjáti H, Walcz I, Virányi F, Zipper R, Thines M, Spring O, 2007. Characteristics of a Plasmopara angustiterminalis isolate from Xanthium strumarium. European Journal of Plant Pathology, 119(4):421-428. http://springerlink.metapress.com/link.asp?id=100265
  5. Walcz I, Bogßr K, Virßnyi F, 2000. Study on an Ambrosia isolate of Plasmopara halstedii. Helia, 23(33):19-24; 8 ref.
  6. 1 2 3 Sackston, W.E. (1981) Downy mildew of sunflower. In: The Downy Mildews (Spencer, D.M., ed.), pp. 545–575.London: Academic Press.
  7. Mouzeyar, S., Tourvieille de Labrouhe, D. and Vear, F. (1993) Histopathological studies of resistance of sunflower (Helianthus annuus L.) to downy mildew (Plasmopara halstedii). J. Phytopathol. 139, 289–297.
  8. 1 2 Gulya, T.J., Tourvieille de Labrouhe, D., Masirevic, S., Penaud, A., Rashid, K. and Viranyi, F. (1998) Proposal for the standardized nomenclature and identification of races of Plasmopara halstedii (sunflower downy mildew). In: Sunflower Downy Mildew Symposium, Proceedings of Sunflower Downy Mildew Symposium, International Sunflower Association Symposium III, Fargo, ND, USA, pp. 130–136.
  9. Ioos, R., Laugustin, L., Rose, S., Tourvieille, J. and de Labrouhe, D.T. (2007) Development of a PCR test to detect the downy mildew causal agent Plasmopara halstedii in sunflower seeds. Plant Pathol.56, 209–218.
  10. 1 2 3 Spring, O. and Zipper, R. (2000) Isolation of oospores of sunflower downy mildew, Plasmopara halstedii, and microscopical studies on oospore germination. J. Phytopathol. 148, 227–231.
  11. Grenville-Briggs, L.J. and Van West, P. (2005) The biotrophic stages of oomycete–plant interactions. Adv. Appl. Microbiol. 57, 217–243.
  12. Spring, O. (2000) Homothallic sexual reproduction in Plasmopara halstedii, the downy mildew of sunflower.Helia, 23, 19–26.
  13. 1 2 Gulya, T.J.; Sackston, W.E.; Virányi, F.; Masirevic, S.; Rashid, K.Y. (1991) New races of the sunflower downy mildew pathogen (Plasmopara halstedii) in Europe and North and South America. Journal of Phytopathology 132, 303-311.
  14. 1 2 Sackston WE, 1992. On a treadmill: breeding sunflowers for resistance to disease. Annual Review of Phytopathology, 30:529-551; 123 ref.
  15. Skoric D, 1994. Sunflower breeding for resistance to dominant diseases. In: Proceedings of the EUCARPIA Oil and Protein Crops Section, Symposium on Breeding of Oil and Protein Crops, Albena, Bulgaria, 30-48.
  16. Achbani EH, Lamrhari A, Serrhini MN, Douira A, Tourvieille de Labrouche D, 1999. Evaluation of the efficacy of seed treatments against Plasmopara halstedii. Bulletin OEPP, 29(4):443-449; 15 ref.
  17. Oros G, Viranyi F, 1987. Glasshouse evaluation of fungicides for the control of sunflower downy mildew (Plasmopara halstedii). Annals of Applied Biology, 110(1): 53-63.
  18. Lafon S, Penaud A, Walser P, De Guenin M-Ch, Molinero V, Mestres R, Tourvieille D, 1996. Le mildiou du tournesol toujour sou surveillance. Phytoma, 484:35-36.
  19. Nandeeshkumar P, Ramachandra K, Prakash HS, Niranjana SR, Shetty H, 2008. Induction of resistance against downy mildew on sunflower by rhizobacteria, 3(4):255-262.
  20. Anon. (1981) Sunflower downy mildew. Plant Quarantine Leaflet No. 13. Commonwealth Department of Health, Canberra, Australia.

External links

Further reading

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