Oral Technical Session: Mechanism of Host and Non-Host Resistance

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The role of AtBAG6 as a positive regulator of autophagy in fungal pathogen resistance.
Y. LI (1), M. Kabbage (2), M. Dickman (1)
(1) Texas A&M University, College Station, TX, U.S.A.; (2) University of Wisconsin, Madison, WI, U.S.A.

The BAG (Bcl-2-associated athanogene) family function as co-chaperones that modulate diverse cellular processes ranging from proliferation to growth arrest and cell death in both plants and animals. Bioinformatic approaches uncovered the Arabidopsis BAG gene family. Our recent studies focus on AtBAG6. AtBAG6 knockout lines resulted in a dramatic loss of non-host resistance in Arabidopsis to the necrotrophic fungal pathogen Botrytis cinerea. Expression of full length AtBAG6 had no adverse effects on host plants or in yeast two hybrid studies; however expression of the AtBAG6, BAG domain alone resulted in both yeast and plant cell death. Overexpression of AtBAG6 exhibited a lesion mimic phenotype, while localization studies indicated that AtBAG6 resides in the vacuole. We identified a predicted caspase-1 cleavage site in AtBAG6, suggesting AtBAG6 needs processing for cell death/cytoprotective activity. Human Caspase-1 cleaved this site as predicted and chitin treatment or Botrytis cinerea inoculation, also demonstrated cleavage of this site. Site directed mutation of this site abolished cleavage. When the processed form of AtBAG6 was transiently expressed in tobacco, autophagy was observed. Collectively, these results suggest that AtBAG6 is processed following Botrytis challenge; presumably via a caspase-1 like protease. This processing is necessary for defense associated autophagy, resistricting fungal growth and spread.