Spatiotemporal patterns of oxidative burst and micronecrosis in resistance of wheat to brown rust infection

Abstract

The accumulation of H 2 O 2 (oxidative burst) and the progress of pathogen development were studied in compatible and incompatible wheat-brown rust interactions. The accumulation of H 2 O 2 was detected in 98AE7% of guard cells with appressoria 8 h post inoculation (hpi). The reaction in both susceptible and resistant plants declined 2-3 days post inoculation (dpi). The second phase of the oxidative burst was observed in the mesophyll and ⁄ or epidermis. In susceptible plants it began 4-5 dpi and was detected only in the epidermis. In resistant plants the response was observed in the mesophyll. In moderately resistant plants it was induced 1-3 dpi, and the percentage of infection units reached 80-90% 8 dpi. This corresponded with severe necrotic symptoms. In highly resistant plants, the oxidative burst was short and transient. The percentage of infection units with H 2 O 2 accumulation reached its highest level (60-70%) 2 dpi, and decreased thereafter. Four days later, the low percentage and weak DAB staining indicated very low H 2 O 2 accumulation. The localization and the time-course changes of the oxidative burst correlated with the profiles of the micronecrotic response, haustorium mother cell formation and pathogen development termination. An early and localized induction of oxidative burst followed by its rapid quenching correlated with high resistance and almost no disease symptoms. The possible correlation of the oxidative burst and pathogen development patterns with the level and durability of resistance conferred by Lr genes are discussed.

Histological and molecular studies of the non-host interaction between wheat and Uromyces fabae

“…TaPR1, pathogenesis-related protein 1 (AAK60565); TaPR2, -1,3-glucanase (DQ090946); TaPR3, chitinase (TC369412); TaPR5, thaumatin-like protein (FG618781); TaPAL, phenylalanine ammonia lyase (TC294834); TaSOD, superoxide dismutase (U69632.1); TaCAT, catalase (X94352); and TaAPX, ascorbate-peroxidase, (TC369354) Hours after inoculation Relative expression haustorium encasement. Consistent with previous studies (Wang et al 2007;Orczyk et al 2010), our results indicate that accumulation of H 2 O 2 in guard cells was a common defensive reaction in wheat against rust fungi, including non-adapted species such as Uf. As reported in host and non-host interactions of cereal plants with the powdery mildew fungus (Thordal-Christensen et al 1997;Huckelhoven et al 2001), the cross-link fueled by H 2 O 2 likely reinforces the cell wall at the sites in contact with fungal structures and strengthening papillae as well as the encasement of haustoria and results in the arrest of Uf growth in wheat.…”

“…Generation and accumulation of ROS, such as hydrogen peroxide (H 2 O 2 ) and superoxide anion (O 2 ¡ ) at the penetration sites are often associated with early host defense responses (Thordal-Christensen et al 1997). Oxidative burst and ROS accumulation have been shown to be important for resistance against rust fungi in wheat (Wang et al 2007;Orczyk et al 2010). In responses to Uf infection, accumulation of H 2 O 2 , but not O 2 ¡ , was detected in wheat cells.…”

TaMCA1, a regulator of cell death, is important for the interaction between wheat and Puccinia striiformis

“…ROS accumulation in host cells is a plant defense response that is important for resistance against rust fungi in wheat383940. In this study, the transcript levels of TaCAT , TaPOD and TaSOD were down-regulated in TaMCA1-knockdown plant after infection with Pst , especially at 24 hpi.…”

Microscopy and proteomic analysis of the non-host resistance of Oryza sativa to the wheat leaf rust fungus, Puccinia triticina f. sp. tritici

“…H 2 O 2 accumulation was also observed in wheat epidermal cells during resistance to incompatible races of Ptt (Orczyk et al 2010) and arabidopsis epidermal cells during NHR to Ptt or P. pachyrhizi (Loehrer et al 2008;Shafiei et al 2007 (Jeun et al 2004). As fluorescence occurred in cells not directly contacting the pathogen, the contacted cells or fungus may have transmitted a signal to nearby cells to activate this response.…”