Abstract
Biotrophic pathogens, like the powdery mildew fungi, require living plant cells for their growth and reproduction. During infection, a specialized structure called the haustorium is formed by the fungus. The haustorium is surrounded by a plant cell-derived extrahaustorial membrane (EHM). Over the EHM, the fungus obtains nutrients from and secretes effector proteins into the plant cell. In the plant cell these effectors interfere with cellular processes such as pathogen defense and membrane trafficking. However, the mechanisms behind effector delivery are largely unknown. This paper provides a model for and new insights into a putative transfer mechanism of effectors into the plant cell. We show that silencing of the barley Sec61βa transcript results in decreased susceptibility to the powdery mildew fungus. HvSec61βa is a component of both the endoplasmic reticulum (ER) translocon and retrotranslocon pores, the latter being part of the ER-associated protein degradation machinery. We provide support for a model suggesting that the retrotranslocon function of HvSec61βa is required for successful powdery mildew fungal infection. HvSec61βa-GFP and a luminal ER marker were co-localized to the ER, which was found to be in close proximity to the EHM around the haustorial body, but not the haustorial fingers. This differential EHM proximity suggests that the ER, including HvSec61βa, may be actively recruited by the haustorium, potentially to provide efficient effector transfer to the cytosol. Effector transport across this EHM-ER interface may occur by a vesicle-mediated process, while the Sec61 retrotranslocon pore potentially provides an escape route for these proteins to reach the cytosol.
Highlights
Many filamentous plant pathogenic fungi and oomycetes rely on placing a feeding structure, a so-called haustorium inside host cells in order to exploit host resources and to transfer effector proteins to the host cytosol
Five days after transformation together with a reference construct for cytosolic mCherry expression, confocal imaging revealed that the RNA interference (RNAi) construct prevented appearance of GFP signal, while it did not affect the signal from mCherry in the same cell (Figure 1B)
The fact that silencing of HvSec61βa causes the barley cells to become resistant to powdery mildew suggests that HvSec61βa either is a negative regulator of defense or a susceptibility factor required for disease
Summary
Many filamentous plant pathogenic fungi and oomycetes rely on placing a feeding structure, a so-called haustorium inside host cells in order to exploit host resources and to transfer effector proteins to the host cytosol. By unknown mechanisms, these pathogens trigger the host cells to generate an extrahaustorial membrane (EHM), which allows the host cells to stay alive despite the severe haustorial invasions (Gan et al, 2012). In between the haustorium and the EHM, a sealed compartment, called the extrahaustorial matrix (EHMx) is present Many of these pathogens, such as powdery mildew fungi, have genetically lost certain general lifesustaining processes during their evolution (Spanu et al, 2010). This motif guides the effectors to be transported across membranes and allows them to enter the host cytosol (Whisson et al, 2007)
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