TY - JOUR
T1 - Initiation of RPS2-specified disease resistance in Arabidopsis is coupled to the AvrRpt2-directed elimination of RIN4
AU - Axtell, Michael J.
AU - Staskawicz, Brian J.
N1 - Funding Information:
We thank Alison Davis, Stephen Chisholm, Brad Day, Todd Leister, and Mary Beth Mudgett for thoughtful and incisive comments during manuscript production; Jeff Dangl and David Mackey for generous sharing of antisera, transgenic T7-RIN4 plants, and many enlightening discussions; Barbara Kunkel for the gift of AvrRpt2 expressing transgenic plants; Andrew Jackson for the use of his ultracentrifuge; and Rob Jensen, Phil Rea, Sally Rogers, and John Sedbrook for gifts of antibodies. M.J.A. is supported by a NSF Graduate Research Fellowship; B.J.S. is currently a Miller Research Professor supported by the Miller Institute for Basic Research in Science at UC Berkeley. This work was supported by DOE grant DE-FG03-88ER13917 to B.J.S.
PY - 2003/2/7
Y1 - 2003/2/7
N2 - Plants have evolved a sophisticated innate immune system to recognize invading pathogens and to induce a set of host defense mechanisms resulting in disease resistance. Pathogen recognition is often mediated by plant disease resistance (R) proteins that respond specifically to one or a few pathogen-derived molecules. This specificity has led to suggestions of a receptor-ligand mode of R protein function. Delivery of the bacterial effector protein AvrRpt2 by Pseudomonas syringae specifically induces disease resistance in Arabidopsis plants expressing the RPS2 R protein. We demonstrate that RPS2 physically interacts with Arabidopsis RIN4 and that AvrRpt2 causes the elimination of RIN4 during activation of the RPS2 pathway. AvrRpt2-mediated RIN4 elimination also occurs in the rps2, ndr1, and Atrar1 mutant backgrounds, demonstrating that this activity can be achieved independent of an RPS2-mediated signaling pathway. Therefore, we suggest that RPS2 initiates signaling based upon perception of RIN4 disappearance rather than direct recognition of AvrRpt2.
AB - Plants have evolved a sophisticated innate immune system to recognize invading pathogens and to induce a set of host defense mechanisms resulting in disease resistance. Pathogen recognition is often mediated by plant disease resistance (R) proteins that respond specifically to one or a few pathogen-derived molecules. This specificity has led to suggestions of a receptor-ligand mode of R protein function. Delivery of the bacterial effector protein AvrRpt2 by Pseudomonas syringae specifically induces disease resistance in Arabidopsis plants expressing the RPS2 R protein. We demonstrate that RPS2 physically interacts with Arabidopsis RIN4 and that AvrRpt2 causes the elimination of RIN4 during activation of the RPS2 pathway. AvrRpt2-mediated RIN4 elimination also occurs in the rps2, ndr1, and Atrar1 mutant backgrounds, demonstrating that this activity can be achieved independent of an RPS2-mediated signaling pathway. Therefore, we suggest that RPS2 initiates signaling based upon perception of RIN4 disappearance rather than direct recognition of AvrRpt2.
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U2 - 10.1016/S0092-8674(03)00036-9
DO - 10.1016/S0092-8674(03)00036-9
M3 - Article
C2 - 12581526
AN - SCOPUS:0037423390
SN - 0092-8674
VL - 112
SP - 369
EP - 377
JO - Cell
JF - Cell
IS - 3
ER -