Abstract
Programmed cell death often depends on generation of reactive oxygen species, which can be detoxified by antioxidative enzymes, including catalases. We previously isolated catalase-deficient mutants (cat2) in a screen for resistance to hydroxyurea-induced cell death. Here, we identify an Arabidopsis thaliana hydroxyurea-resistant autophagy mutant, atg2, which also shows reduced sensitivity to cell death triggered by the bacterial effector avrRpm1. To test if catalase deficiency likewise affected both hydroxyurea and avrRpm1 sensitivity, we selected mutants with extremely low catalase activities and showed that they carried mutations in a gene that we named NO CATALASE ACTIVITY1 (NCA1). nca1 mutants showed severely reduced activities of all three catalase isoforms in Arabidopsis, and loss of NCA1 function led to strong suppression of RPM1-triggered cell death. Basal and starvation-induced autophagy appeared normal in the nca1 and cat2 mutants. By contrast, autophagic degradation induced by avrRpm1 challenge was compromised, indicating that catalase acted upstream of immunity-triggered autophagy. The direct interaction of catalase with reactive oxygen species could allow catalase to act as a molecular link between reactive oxygen species and the promotion of autophagy-dependent cell death.
Highlights
Programmed cell death (PCD) is a necessary part of the life of multicellular organisms
To cat2 mutants, the nca1 mutants were resistant to hydroxyurea (Figure 2A) and showed reduced growth at ambient CO2 levels (Figure 2B), which could be rescued by increasing the CO2 concentration (Figure 2C)
The amount of catalase protein was markedly decreased in both nca1 mutants (Figure 2F) and the enzymatic activity of all three catalase isoforms was clearly decreased (Figure 2G), indicating that NO CATALASE ACTIVITY1 (NCA1) is required for the activity of all Arabidopsis catalases and acts mainly at the posttranscriptional level
Summary
Programmed cell death (PCD) is a necessary part of the life of multicellular organisms. It is associated with normal development and with immune responses aimed at pathogen clearance and destruction of otherwise harmful cells. Plant and animal innate immune systems detect conserved microbe-associated molecular patterns, such as flagellin-derived peptides, using pattern recognition receptors (Ausubel, 2005). To circumvent this detection system, adapted plant pathogens inject effectors directly into plant cells. Plant immune receptors known as R proteins detect the presence of effectors. This recognition leads to effector-triggered immunity, which often culminates in a hypersensitive response (HR) leading to accumulation of reactive oxygen species (ROS) and PCD (Jones and Dangl, 2006)
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