Pathogen

Wheat blast is caused by Magnaporthe oryzae pathotype Triticum (MoT) (Maciel, 2016; Castroagudin et al., 2015, Perello et al., 2015; Maciel et al., 2014). Since the disease is of recent origin, researchers refer to the pathogen variously as Pyricularia grisea (Filha et al., 2011; Kohli et al., 2011; Rocha et al., 2014). Pyricularia oryzae (Araujo et al., 2016; Oliveira et al., 2015; Cruz et al., 2015a; Silva et al., 2015), Magnaporthe grisea (Urashima & Kato, 1994; Peng et al., 2011; Pagani et al., 2014) and M. oryzae Triticum (Cruz et al., 2015b). The blast pathogen has been observed to have a wide host range and is known to infect many cereals such as rice, wheat and barley, as well as grasses. The pathotypes of MoT are a subpopulation within M. oryzae and are different from subpopulations infecting other cereals such as rice (the Oryzae pathotypes, MoO), finger millet (the Eleusine pathotypes) and foxtail millet (the Setaria pathotypes). However, the wheat blast pathogen differs from the rice-blast pathogen in terms of inheritance of pathogenicity (Urashima, 1999). Oh et al. (2002) discovered a temperature-dependent virulence of an Avena isolate on wheat. Wheat was susceptible to this isolate at 28°C but became resistant at 20°C. This temperature-dependent resistance was found to be associated with an increased incidence of papilla formation and a hypersensitive reaction (HR). Previous to this study, Urashima and Kato (1998) in a greenhouse study had reported the role of the development stage in blast disease in cross-inoculation studies. Wheat was susceptible to blast strain from Setaria geniculate at seedling stage, but was resistant at the adult plant stage. In contrast, wheat was resistant to the strain from Brachiaria plantaginea at seedling stage, but was susceptible at the adult plant stage. The super pathogen complex of M. oryzae-M. grisea comprises several host-specific subgroups virulent on several species, but there is no barley-specific subgroup. To characterise the relationship between barley and various subgroups of the pathogen, Hyon et al. (2012) inoculated 24 barley cultivars with each of 18 isolates from various hosts. The cultivar-pathogen interaction ranged from non-host-like immune responses to typical host responses. At the gene level, the immune response emanated from the gene PWT1, whereas at the cytological level, the immune response was associated with both papilla formation and hypersensitive reaction. The authors opined that these interactions could reveal various steps in the process of host specialisation of a parasite species and the concomitant evolution of resistance. Klaubauf et al. (2014) attempted to clarify the taxonomic relationship among species that are Magnaporthe or Pyricularia like in morphology. They proposed 10 novel genera and 7 novel species, and also concluded that neither host range can be used as a taxonomic criterion without extensive pathotyp-ing nor can the conidium morphology be used as a taxonomic criterion at the generic level without phylogenetic data.

The blast pathogen can spread through seed and can survive on crop residues. An infected rachis passes on the pathogen to the harvested seed. Goulart et al. (1995) found that no seed from variety BH1146 carried the blast pathogen as this variety had the least infection index contrary to the variety Anahuac that had highest infection index (99.5%) with 26.7% of its seeds carrying the wheat blast pathogen. They also reported a significant positive correlation between the field incidence of wheat blast and the percentage of seed-carrying blast pathogen. A study involving the riceblast pathogen revealed that crop residue was a more efficient source of inoculum as compared to seed (Raj & Pannu, 2017).

 
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