Blumeria graminis

The genomes of B. g. f. sp. hordei[5] and B. g. f. sp. tritici have recently been sequenced.[6] Sequencing of the genome of the wheat powdery mildew B. g. f. sp. tritici, has allowed inference of important aspects of its evolution. It has been seen that it is the most repetitive fungal genome sequenced as of March 2013 with 90% transposable elements. Additionally, 6540 genes were annotated, from which 437 encoded candidate secretor proteins and 165 for non-secreted candidate secretor proteins. These were shown to be subject to positive selection, due to their implication in the gene-for-gene relationship to defeat plant disease resistance. The ability to infect tetraploid- as well as domesticated hexaploid wheat, was seen to be the result of mildew genomes being mosaics of ancient haplogroups that existed before wheat domestication. This has allowed wheat powdery mildew to maintain genetic flexibility, variability and thus a great potential for pathogen variation. It is hypothesized that this mosacisism can be maintained through clonal reproduction in populations with a small effective size or quasi-clonal reproduction in populations with large effective size.

Wheat powdery mildew is an obligate biotroph with a poorly understood evolutionary history. Sequencing its genome in 2013, many aspects of the evolution of its parasitism were unveiled.[7] Obligate biotrophy has appeared multiple times in evolution in both ascomycetes like B. graminis and basidiomycetes, thus different selective pressure must have acted in the different organisms through time. It has been seen that B. g. f.sp. tritici's genome is a mosaic of haplogroups with different divergence times, which explains its unique pathogen adaptability. Haplogroup H_old (diverged 40-80 mya) allows for the infection of wild tetraploid wheat and H_young (diverged 2-10 mya) allows for the infection of both domesticated hexaploid wheat species. Additionally, it has been seen that there is a positive selective pressure acting on genes that code for candidate secretor proteins and non-secreted candidate secretor proteins, indicating that these might participate in the gene-for-gene relationship of plant disease resistance.

Triticum spp. (wheat) is the only host of B. g. f. sp. tritici.[8] Signs on the foliage of wheat are white, powdery mycelium and conidia.[10] As the disease progresses, the patches turn gray and small dark black or brown cleistothecia form in the mycelium mass.[11] Symptoms progress from lower to upper leaves. Symptoms of powdery mildew are chlorotic areas surrounding the infected areas.[10] The lower leaf surface corresponding to the mycelial mat will also show chlorosis.[11] Lower leaves are commonly the most infected because of higher humidity around them.[8]

B. g. f. sp. tritici has a polycyclic life cycle typical of its phylum, Ascomycota. Powdery mildew of wheat overwinters as cleistothecia dormant in plant debris. Under warmer conditions, however, the fungus can overwinter as asexual conidia or mycelium on living host plants. It can persist between seasons most likely as ascospores in wheat debris left in the field. Ascospores are sexual spores produced from the cleistothecia. These spores, as well as conidia, serve as the primary inoculum and are dispersed by wind. Neither spore requires free water to germinate, only high relative humidity.[11] Wheat powdery mildew thrives in cool humid conditions and cloudy weather increases chances of disease. When conidia land on a wheat leaf's hydrophobic surface cuticle, they release proteins which facilitate active transport of lightweight anions between leaf and fungus even before germination. This process helps Blumeria recognize that it is on the correct host and directs growth of the germ tube.[12] Both ascospores and conidia germinate directly with a germ tube. Conidia can recognize the host plant and within one minute of initial contact, the direction of germ tube growth is determined. The development of appressoria then begins infection following the growth of a germ tube.[13] After initial infection, the fungus produces haustoria inside of the wheat cells and mycelium grows on the plant's outer surface.[11] Powdery mildew of wheat produces conidia during the growing season as often as every 7 to 10 days.[14] These conidia function as secondary inoculum as growth and reproduction repeat throughout the growing season.

Powdery mildew of wheat thrives in cool, humid climates and proliferates in cloudy weather conditions.[15] The pathogen can also be an issue in drier climates if wheat fields are irrigated.[16] Ideal temperatures for growth and reproduction of the pathogen are between 60 °F (16 °C) and 70 °F (21 °C) with growth ceasing above 77 °F (25 °C). Dense, genetically similar plantings provide opportune conditions for growth of powdery mildew.[11]

Controlling the disease involves eliminating conducive conditions as much as possible by altering planting density and carefully timing applications and rates of nitrogen. Since nitrogen fertilizers encourage dense leafy growth, nitrogen should be applied at precise rates, less than 70 pounds per acre, to control decrease severity. Crop rotation with non-host plants is another way to keep mildew infection to a minimum, however the aerial nature of conidia and ascospore dispersal makes it of limited use. Wheat powdery mildew can also be controlled by eliminating the presence of volunteer wheat in agricultural fields as well as tilling under crop residues.[14]

Chemical control is possible with fungicides such as triadimefon and propiconazole. Another chemical treatment involves treating wheat with a silicon solution or calcium silicate slag. Silicon helps the plant cells defend against fungal attack by degrading haustoria and by producing callose and papilla. With silicon treatment, epidermal cells are less susceptible to powdery mildew of wheat.[17]

Milk has long been popular with home gardeners and small-scale organic growers as a treatment for powdery mildew. Milk is diluted with water (typically 1:10) and sprayed on susceptible plants at the first sign of infection, or as a preventative measure, with repeated weekly application often controlling or eliminating the disease. Studies have shown milk's effectiveness as comparable to some conventional fungicides,[18] and better than benomyl and fenarimol at higher concentrations.[19] Milk has proven effective in treating powdery mildew of summer squash,[19] pumpkins,[18] grapes,[20] and roses.[20] The exact mechanism of action is unknown, but one known effect is that ferroglobulin, a protein in whey, produces oxygen radicals when exposed to sunlight, and contact with these radicals is damaging to the fungus.[20]

Another way to control wheat powdery mildew is breeding in genetic resistance, using "R genes" (resistance genes) to prevent infection. There are at least 25 loci on the wheat genome that encode resistance to powdery mildew. If the particular variety of wheat has only one loci for resistance, the pathogen may be controlled only for a couple years. If, however, the variety of wheat has multiple loci for resistance, the crop may be protected for around 15 years. Because finding these loci can be difficult and time-consuming, molecular markers are used to facilitate combining resistant genomes.[15] One organization working towards identifying these molecular markers is the Coordinated Agricultural Project for Wheat . With these markers established, researchers will then be able to determine the most effective combination of resistance genes.[21]

HSP70-4 is an HSP70 – a family of heat shock proteins – in Arabidopsis.[22] The ortholog HvHSP70-4 in barley (Hordeum vulgare) is disclosed by Molitor et al., 2011.[22] They find that it is transcribed in response to B. graminis infection, is protective against Bg infection, and that prophylactic infection with Piriformospora indica produces systemic induced resistsance to Bg.[22]

Powdery mildew can be found in all wheat growing areas of the United States but usually will be most severe in the east and southeast.[11] It is more common in areas with a humid or semi-arid environment where wheat is grown.[11] Powdery mildew has become a more important disease in some areas because of increased application of nitrogen fertilizer, which favors the development of the fungus.[10] Severe symptoms of powdery mildew can cause stunting of wheat.[10] If unmanaged, this disease can reduce yields significantly by reducing photosynthetic areas and causes non-seed producing tillers.[8] Powdery mildew causes reduced kernel size and lower yields.[14] The sooner powdery mildew begins to develop and how high on the plant it develops by flowering the larger the yield loss.[14] Yield Losses up to 45 percent have been shown in Ohio on susceptible varieties when plants are infected early and weather favors disease.[14]