Disease relevance of PAD4

• 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 [1].
• Both PAD4 and NahG acted epistatically to SID regarding the Pst-dependent production of ET that was found to be necessary for the accumulation of camalexin [2].

High impact information on PAD4

• Epistatic analysis showed that the SA-dependent pathways require two regulators of SA-mediated resistance responses, PAD4 and EDS1 [3].
• Direct interaction between the Arabidopsis disease resistance signaling proteins, EDS1 and PAD4 [4].
• However, EDS1 dimerization is mediated by different domains to those involved in EDS1-PAD4 association [4].
• These results demonstrate that NDR1, EDS1, and PAD4 mediate other resistance signaling function(s) in addition to salicylic acid and pathogenesis-related protein accumulation [5].
• In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates [6].

Biological context of PAD4

• Taken together, these results demonstrate that SIZ1 is required for SA and PAD4-mediated R gene signalling, which in turn confers innate immunity in Arabidopsis [7].
• An Arabidopsis whole genome microarray experiment was designed to identify genes whose expression depends on EDS1 and PAD4, irrespective of local SA accumulation, and potential candidates of an SA-independent branch of EDS1 defense were found [6].
• Thus SA, NPR1, and PAD4 are required for the phenotypes [8].
• The disease resistance signaling components EDS1 and PAD4 are essential regulators of the cell death pathway controlled by LSD1 in Arabidopsis [9].
• The combined activities of SAG101 and PAD4 are necessary for programmed cell death triggered by the Toll-Interleukin-1 Receptor type of nucleotide binding/leucine-rich repeat immune receptor in response to avirulent pathogen isolates and in restricting the growth of normally virulent pathogens [10].

Associations of PAD4 with chemical compounds

• EDS1 is essential for elaboration of the plant hypersensitive response, whereas EDS1 and PAD4 are both required for accumulation of the plant defence-potentiating molecule, salicylic acid [4].
• Arabidopsis MAP kinase 4 regulates salicylic acid- and jasmonic acid/ethylene-dependent responses via EDS1 and PAD4 [11].
• The expression of PAD3 is tightly correlated with camalexin synthesis and is regulated by PAD4 and PAD1 [12].
• The predicted PAD4 protein sequence displays similarity to triacyl glycerol lipases and other esterases [13].
• NahG plants and pad4 mutants were also found to produce less ethylene (ET) after infection with Pst in comparison to the wild type (WT) and sid mutants [2].

Physical interactions of PAD4

• Yeast two-hybrid analysis reveals that EDS1 can dimerize and interact with PAD4 [4].

Other interactions of PAD4

• Co-immunoprecipitation experiments show that EDS1 and PAD4 proteins interact in healthy and pathogen-challenged plant cells [4].
• Together, EDS1, PAD4 and SAG101 provide a major barrier to infection by both host-adapted and non-host pathogens [14].
• The enhanced resistance is mediated by salicylic acid, PAD4 and a disease resistance gene SNC1 [15].
• High levels of SA upregulate HRT expression via a PAD4-dependent pathway [16].
• Several other genes with regulatory functions have been identified by mutation, including DND1, PAD4, CPR6, and SSl1 [17].

References