Special Plant Seminar June 2017

30.6.2017
Hans Thordal-Christensen, University of Copenhagen, Denmark

Date: 30th June 2017

Time: 10:45

Title: Membrane trafficking in plant cells attacked by powdery mildew fungi

Location: Auditorium 2, Viikki Korona Info building, Viikinkaari 11

Host: Kurt Fagerstedt

Abstract: We are interested in plant membrane trafficking processes and how they are involved in plant interactions with microbes. For this purpose, we use the powdery mildew fungi and the attacked leaf epidermal cells, which are amenable for confocal microscopy. These fungi are obligate biotrophs, introducing haustoria in the host cell as a means of acquiring nutrients.

We have previously shown that the syntaxin, PEN1, is required for plant defence against penetration and haustoria establishment. Later, we found that treatment with Brefeldin A (BFA) hampers penetration resistance. BFA suppresses a subset of the plant’s ARF GTPase guanine nucleotide exchange factors (GEFs), which regulate membrane budding. A well-studied BFA-sensitive ARF GEF is GNOM. By introducing a mutant version of GNOM, which is insensitive to BFA, we could show that GNOM is the ARF GEF that is essential for penetration resistance. A defence component, which is often observed but poorly studied, is the haustorial encasement. Here a cell wall-like structure forms around the haustorium. We have uncovered a Rab GTPase involved in encasement formation and been able to document that this structure suppresses pathogen proliferation. Pathogen haustoria are surrounded by plant-generated membranes. The nature of these extrahaustorial membranes (EHM) remains enigmatic. We have addressed this question and found that the powdery mildew-associated EHM in barley cells shares features with the endoplasmic reticulum membrane (ER), although the EHM is not an extension of the ER.

Hans Thordal-Christensen's group focuses on molecular and cellular studies of how powdery mildew fungal pathogens are established in the plant cell and how plants defend themselves against their attack.

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