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4月7日清华大学生物论坛-Martin B. Dickman
发布时间:2015-04-02关键字:

 Tipping the Balance: Cell Death Control

in Plant-Pathogen Interactions


Martin B. Dickman PhD
Department of Plant Pathology & Microbiology Center
Texas A&M University

Abstract:Programmed cell death is characterized by a cascade of tightly controlled events that culminate in the orchestrated death of the cell. In multicellular organisms, autophagy and apoptosis are recognized as two principal means by which these genetically determined cell deaths occur. During plant-microbe interactions cell death programs can mediate both resistant and susceptible responses in the host. Via oxalic acid (OA), the necrotrophic phytopathogen, Sclerotinia sclerotiorum hijacks host pathways and induces cell death in host plant tissue resulting in hallmark apoptotic features in a time and dose dependent manner. OA deficient mutants are non-pathogenic and trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive response including callose deposition and a pronounced oxidative burst, suggesting the plant can recognize and in this case, respond, defensively. Using a combination of electron and fluorescence microscopy, chemical effectors and reverse genetics, we will show that this constrained cell death is autophagic. Inhibition of autophagy rescues the non-pathogenic mutant phenotype. These findings suggest that autophagy is a defense response in this necrotrophic fungus/plant interaction and point towards a novel function associated with OA; namely; the suppression of autophagy. These data suggest that not all cell deaths are equivalent, and though programmed cell death occurs in several situations, the outcome is predicated on which party is in control of the cell death machinery. Based on our data, we suggest that it is not cell death per se that dictates the outcome of certain plant-microbe interactions, but the manner by which cell death occurs, that is crucial.
The Bcl-2-associated-athanogene (BAG) family is an evolutionarily conserved group of co-chaperones that modulate numerous cellular processes in plants and animals. This family was uncovered in a search for plant homologs of mammalian genes that modulate PCD. Using  bioinformatics tools generating predictions based on structural similarities, independent of sequence we found uncovered the Arabidopsis gene family. We will show that one family  member, AtBAG6, is required for basal immunity against the fungal phytopathogen Botrytis cinerea. However, the mechanism(s) by which AtBAG6 controls immunity are not clear. We describe results of experiments that determine the molecular mechanisms responsible for AtBAG6 mediated basal resistance. We show that AtBAG6 is cleaved in vivo in a caspase-1 dependent manner, and by a combination of pull-downs, mass spectrometry, yeast-two-hybrid and chemical genomics, we demonstrate that AtBAG6 interacts with a C2 GRAM domain protein (AtBAGP1) and a novel aspartyl protease (AtAPCB1), both of which are required for AtBAG6 processing. Furthermore, AtBAG6 cleavage triggers autophagy in the host that coincides with disease resistance. Targeted inactivation of AtBAGP1 or AtAPCB1 results in the blocking autophagy and loss of resistance. Further, mutation of the cleavage site also blocks the induction of autophagy and resistance. Taken together, these results couple a novel aspartyl protease with a molecular co-chaperone to trigger autophagy, plant defense, and provide a key link between fungal recognition and the induction of cell death and resistance. 


Time: Apr.7th.2015,16:00
Venue: New Biology Buliding,Room 143
Host: Prof.Yule Liu
举办单位:生命科学联合中心
 
 

 




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