Holger Schultheiss, and
First and sixth authors: Lehrstuhl für Phytopathologie, Technische Universität München, 85350 Freising-Weihenstephan, Germany; second and third authors: Institute for Biology III (Plant Physiology), RWTH Aachen, D-52056 Aachen, Germany; and fourth and fifth authors: BASF Plant Science GmbH, Agricultural Center, 67117 Limburgerhof, Germany. C. Hoefle and M. Loehrer contributed equally to this study.
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Accepted for publication 10 November 2008.
The basidiomycete Phakopsora pachyrhizi (P. pachyrhizi) causes Asian soybean rust, one of the most devastating plant diseases on soybean. When inoculated on the nonhost barley P. pachyrhizi caused only very small necrotic spots, typical for an incompatible interaction, which involves a hypersensitive cell death reaction. A microscopic inspection of the interaction of barley with P. pachyrhizi revealed that the fungus germinated on barley and formed functional appressoria on epidermal cells. The fungus attempted to directly penetrate through periclinal cell walls but often failed, arrested in plant cell wall appositions that stained positively for callose. Penetration resistance depends on intact ROR1(REQUIRED FOR mlo-SPECIFIED RESISTANCE 1) and ROR2 genes of barley. If the fungus succeeded in penetration, epidermal cell death took place. Dead epidermal cells did not generally restrict fungal development but allowed for mesophyll invasion, which was followed by mesophyll cell death and fungal arrest. Transient or stable over expression of the barley cell death suppressor BAX inhibitor-1 reduced both epidermal cell death and fungal penetration success. Data suggest that P. pachyrhizi provokes a programmed cell death facilitating fungal entry into epidermal cells of barley.
Additional keywords:hypersensitive reaction, nonhost resistance, transient transformation.
The American Phytopathological Society, 2009