Minisymposium 26: Plant Pathogen Interactions

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Abs # M2604: The Chimeric Cyclic Nucleotide-Gated Ion Channel AtCNGC11/12 Activates Multiple Pathogen Resistance Responses

Presenter:	Yoshioka, Keiko       Contact Presenter
Authors	Yoshioka, Keiko  (A) (B)  Moeder, Wolfgang  (A) (B)  Kang, Hong-Gu  (B)   Kachroo, Pradeep  (B)   Masmoudi, Khaled  (C) (D)  Berkowitz, Gerald  (C)   Klessig, Daniel F (B)
Affiliations:	(A): University of Toronto, Botany Department (B): Boyce Thompson Institute for Plant Research (C): Department of Plant Science, University of Connecticut (D): Center of Biotechnology at Sfax (CBS), Plant Molecular Genetics Unit

To investigate the resistance signaling pathways activated by pathogen infection, we previously identified the Arabidopsis mutant cpr22, which displays constitutive activation of multiple defense responses (Yoshioka et al., 2001). Recently we identify the cpr22 mutation as a 3 kb deletion that fuses two cyclic nucleotide-gated ion channel (CNGC)-encoding genes, AtCNGC11 and AtCNGC12, to generate a novel chimeric gene, AtCNGC11/12. Genetic, molecular and complementation analyses suggest that AtCNGC11/12, as well as AtCNGC11 and AtCNGC12 form functional, cAMP-activated CNGCs, and that the cpr22 phenotype is due to expression of AtCNGC11/12. However, since over-expression of AtCNGC12, but not AtCNGC11, suppressed the cpr22 phenotype, development of this phenotype appears to be regulated by the ratio between AtCNGC11/12 and AtCNGC12. Analysis of knockout lines revealed that both AtCNGC11 and AtCNGC12 are positive mediators of resistance against an avirulent biotype of Hyaloperonospora parasitica. To determine whether cpr22 activates a variety of resistance responses via defense signaling pathways utilized during R gene-mediated resistance, we crossed cpr22 with eds1-1, pad4-1 and ndr1-1 mutants. Through epistatic analyses, cpr22-mediated enhanced resistance to pathogens was found to require both NDR1-dependent and EDS1/PAD4-dependent pathways. In striking contrast, none of these pathways were required for cpr22-induced salicylic acid (SA) accumulation or PR-1 gene expression. These results demonstrate that NDR1, EDS1 and PAD4 mediate other resistance signaling function(s) beside SA and PR protein accumulation. Moreover, the requirement for both NDR1-dependent and EDS1/PAD4-dependent pathways for cpr22-mediated resistance argues that these pathways are cross-regulated.