Infection, Pathogenesis, and Disease Cycle

Abstract

Powdery mildew fungi of crucifers are ectoparasites on their respective host plant species. Primary infection takes place through ascospores or conidia after landing on the host surface through germtube which develops an appressorium at the tip, a thickened infection structure. After cell wall penetration, specialized hyphae feeding structure called haustorium is formed which gets necessary nutrients from the host tissues for the growth, and development of the pathogen to produce mycelium, conidiophores, and conidia to continue its asexual state. Secondary spread of the disease is through air borne conidia causing infection, and pathogenesis under congenial environmental conditions. At the maturity stage of the crop, sexual state of the pathogen is visible in the form of small, pinhead, dark brown spherical chasmothecia which over summer or over winter to serve as a source of primary inoculum for the next season. Chasmothecia imbibe to burst, and release asci, and ascospores which germinate after landing on host surface, and cause primary infection. The pathogenesis of powdery mildew fungi is achieved through the suppression of the hosts preformed, and inducible penetration, resistance mechanisms as well as maintenance of the compatible interaction after host cell penetration. After host cell penetration, the haustorial complex is established, which consists of the fungal haustorium, an extrahaustorial modified plant plasma membrane, and the haustorial matrix. The haustorial complex is the site of the most intimate contact of the pathogen with its host cell, and functions in nutrient uptake, and provides a platform for the delivery of pathogens effector genes for pathogenesis. The expression of hundreds of host genes are altered within 8 hpi indicating that signaling between the pathogen, and individual host cells already occurs a few hours post contact of the powdery mildew conidia or ascospores with the leaf surface of about the stage of penetration, but certainly prior to establishment of the extra- haustorial matrix. For the successful pathogenesis of crucifer's powdery mildew, there is great role of genetic factors (genes), MLO proteins, and host transcriptional changes. Powdery mildew of crucifers is activated by SA signaling pathways at the early stage of infection, and by the JA/ET signaling pathways at the later stage of pathogenesis. Infection is highly activated by chitinase in the genotypes. Adjustment of the plant host metabolism to support the growth of the powdery mildew pathogen is consistent with an increased ploidy level of the mesophyll cells underlying infected epidermal cells. Powdery mildew disease cycle operates at both asexual and sexual stages depending on its host plant species infected under prevailing environmental conditions.