MAPKKKα is a positive regulator of cell death associated with both plant immunity and disease

Abstract

Many plant pathogens cause disease symptoms that manifest over days as regions of localized cell death. Localized cell death (the hypersensitive response; HR) also occurs in disease-resistant plants, but this response appears within hours of attempted infection and may restrict further pathogen growth. We identified a MAP kinase kinase kinase gene (MAPKKKa) that is required for the HR and resistance against Pseudomonas syringae. Significantly, we found that MAPKKKa also regulates cell death in susceptible leaves undergoing P. syringae infection. Overexpression of MAPKKKa in leaves activated MAPKs and caused pathogen-independent cell death. By overexpressing MAPKKKa in leaves and suppressing expression of various MAPKK and MAPK genes by virus-induced gene silencing, we identified two distinct MAPK cascades that act downstream of MAPKKKa. These results demonstrate that signal transduction pathways associated with both plant immunity and disease susceptibility share a common molecular switch.

Eukaryotic Translation Initiation Factor 5A Is Involved in Pathogen-Induced Cell Death and Development of Disease Symptoms in Arabidopsis

“…The level of colonization 24 h after infection reflects initial growth of the pathogen within the apoplast (Katagiri et al, 2002). Subsequent rapid growth of the pathogen over the next 48 h is accompanied by host programmed cell death (Tao et al, 2003;Pozo et al, 2004;Nomura et al, 2005). This pattern of colonization was evident in both wild-type plants and AteIF5A-2-overexpressing plants in this study (Fig.…”

“…For example, early HR-based host cell death and the associated development of systemic acquired resistance following infection with avirulent Pst DC3000 prevent the development of disease symptoms (Katagiri et al, 2002;Pozo et al, 2004). This study indicates that AteIF5A-2 may regulate the induction of this later onset of host cell death that underlies the development of disease symptoms.…”

“…It is generally recognized that signaling associated with a compatible host-pathogen interaction induces programmed cell death (Beers and McDowell, 2001;Greenberg and Yao, 2004;Pozo et al, 2004). Two lines of evidence indicate that AteIF5A-2 plays a role in the induction of programmed cell death following ingression of virulent Pst DC3000 into rosette leaves of Arabidopsis.…”

“…There is evidence that the timing of host programmed cell death induced by facultative necrotrophic pathogens such as Pst DC3000 is a critical determinant of the ensuing disease state (Abramovitch and Martin, 2004;Pozo et al, 2004). For example, early HR-based host cell death and the associated development of systemic acquired resistance following infection with avirulent Pst DC3000 prevent the development of disease symptoms (Katagiri et al, 2002;Pozo et al, 2004).…”

Tomato MAPKs LeMPK1, LeMPK2, and LeMPK3 function in the systemin-mediated defense response against herbivorous insects

“…The corresponding signaling pathways all converge on MPK1, MPK2, and MPK3, which can explain why MPK1/2-silencing prevented a successful defense response against the attacking insect larvae. Overexpression of MPK1/2 orthologs or expression of active forms of their upstream MAPKK(K)s did not lead to JA synthesis (47) and had been shown to mimic pathogen-induced responses or confer resistance to microbial pathogens (43,(48)(49)(50). But no experiments were aimed at testing the performance of chewing insects on such plants.…”