Regulation of appressorium development in pathogenic fungi

Abstract

Many plant pathogenic fungi have the capacity to breach the intact cuticles of their plant hosts using specialised infection cells called appressoria. These cells exert physical force to rupture the plant surface, or deploy enzymes in a focused way to digest the cuticle and plant cell wall. They also provide the means by which focal secretion of effectors occurs at the point of plant infection. Development of appressoria is linked to re-modelling of the actin cytoskeleton, mediated by septin GTPases, and rapid cell wall differentiation. These processes are regulated by perception of plant cell surface components, and starvation stress, but also linked to cell cycle checkpoints that control the overall progression of infection-related development.

Figure 1

Photomicrographs showing appressorium development by the rice blast fungus Magnaporthe oryzae. Conidia were inoculated onto hydrophobic glass coverslips and incubated in a moist chamber at 26 °C for 8 hours. (a) Bright field, epifluorescence and merged images to show localization of the Sep5-GFP septin gene fusion in a hetero-oligomeric ring at the base of the appressorium. The septin ring is necessary for re-modelling F-actin to the appressorium pore [29]. Bar = 10 μm. (b) Septin localization to the appressorium pore is dependent on regulated synthesis of ROS by the Nox2 NADPH oxidase and its regulatory NoxR sub-unit. Sep5-GFP localization in a Δnox1, Δnox2 and ΔnoxR mutant. (c) Nox2-dependent localization of the actin-binding protein gelsolin. Gelsolin-GFP localization in a Δnox1, Δnox2 and ΔnoxR mutant. See [32^•] for details. Bar for (b) and (c) = 5 μm.