ABSTRACT
Background Plants are continuously subjected to pathogen attack and respond by activating a range of defense mechanisms. Recognition of the pathogen or elicitors derived either from the pathogen or released from the plant cell wall is accompanied with the production of molecular signals including salicylic acid [1], jasmonic acid [2] and ethylene [3] that lead to the induction of defense gene expression. is in turn results in the accumulation of functionally diverse pathogenesis-related (PR) proteins and metabolites (e.g., phenylpropanoids) [4,5]. Recognition of the pathogen
or elicitors is usually accompanied by the rapid death of the infected cells, known as the hypersensitive response (HR), which limits the access of the pathogen to water and nutrients thereby restricting its growth [6,7]. HR can be triggered either by non-specic elicitors recognized by plant receptors, or by specic elicitors (encoded by pathogen avirulence (avr) genes) recognized by corresponding encoded products of plant resistance (R) genes [8,9]. Several studies have suggested that plant cell death resulting from the HR is a type of programmed cell death (PCD). Plant cells undergoing PCD share a number of characteristic morphological and biochemical features in common with animal cell apoptosis [7,10,11]. Moreover, cell death with apoptotic features has also been observed in plants susceptible to virulent pathogens [12,13].
