PAD4 Functions Upstream from Salicylic Acid to Control Defense Responses in Arabidopsis

Abstract

The Arabidopsis PAD4 gene was previously shown to be required for synthesis of camalexin in response to infection by the virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326 but not in response to challenge by the non-host fungal pathogen Cochliobolus carbonum. In this study, we show that pad4 mutants exhibit defects in defense responses, including camalexin synthesis and pathogenesis-related PR-1 gene expression, when infected by P. s. maculicola ES4 326. No such defects were observed in response to infection by an isogenic avirulent strain carrying the avirulence gene avrRpt2. In P. s. maculicola ES4 326-infected pad4 plants, synthesis of salicylic acid (SA) was found to be reduced and delayed when compared with SA synthesis in wild-type plants. Moreover, treatment of pad4 plants with SA partially reversed the camalexin deficiency and PR-1 gene expression phenotypes of P. s. maculicola ES4 326-infected pad4 plants. These findings support the hypothesis that PAD4 acts upstream from SA accumulation in regulating defense response expression in plants infected with P. s. maculicola ES4 326. A working model of the role of PAD4 in governing expression of defense responses is presented.

Constitutive disease resistance requires EDS1 in the Arabidopsis mutants cpr1 and cpr6 and is partially EDS1‐dependent in cpr5

“…EDS1-independent signaling may also contribute to the maintenance of constitutive PR2 and PR5 expression in cpr6 eds1 plants. Uncoupling PR1 expression from regulation of PR2 and PR5 mRNAs has been observed in other SA-signaling mutants (Nawrath and Me  traux, 1999;Rogers and Ausubel, 1997;Zhou et al, 1998). Alternatively, residual resistance in cpr6 eds1 may be a consequence of the extremely high PDF1.2 expression observed ( Figure 3a).…”

“…Applications of SA also amplify EDS1 mRNA accumulation, pointing to the existence of an SA-generated positive feedback loop in the defense circuit (Falk et al, 1999). Other Arabidopsis mutations affecting defense signaling upstream of SA accumulation include pad4 (Glazebrook et al, 1997;Zhou et al, 1998), eds5/sid1 and sid2 (Nawrath and Me  traux, 1999;Rogers and Ausubel, 1997). Like EDS1, the wild-type PAD4 gene encodes a lipase-like protein whose expression is ampli®ed by applications of SA (Jirage et al, 1999).…”

Constitutive salicylic acid‐dependent signaling in cpr1 and cpr6 mutants requires PAD4

“…However, the requirement of PAD4 for activation of camalexin synthesis cannot be absolute, as PAD4 is not required for activation of camalexin synthesis after infection by derivatives of P.s. maculicola ES4326 carrying one of the avirulence genes avrRpt2 or avrRpm1 (Zhou et al, 1998). The double mutants were tested for camalexin production after P.s.…”

“…Most of these phenotypes seem to be due to the reduced SA levels in pad4 plants, as they can be largely reversed by treatment with exogenous SA. There must be at least one alternative route leading to activation of SA production in the absence of PAD4, as accumulation of SA, camalexin, and expression of PR-1 in response to activation of some types of gene-for-gene resistance are unaffected by pad4 (Zhou et al, 1998). PAD4 encodes a gene with amino-acid sequence similarity to triacyl glycerol lipases, suggesting that it may be involved in metabolism of a signal molecule (Jirage et al, 1999).…”

“…A gene that is required for gene-for-gene resistance triggered by a subset of R genes, EDS1, also encodes a protein with similarity to triacyl glycerol lipases (Aarts et al, 1998;Falk et al, 1999). Despite their similarity, the functions of PAD4 and EDS1 cannot be redundant, because mutations in either gene cause strong enhanced-susceptibility phenotypes (Aarts et al, 1998;Zhou et al, 1998).…”