Abstract
Programmed cell death (PCD) in plant is triggered by abiotic and biotic stress. Light-dependent PCD is unique to plants. Light-induced PCD also requires reactive oxygen species (ROS) and salicylic acid (SA). In this study, lesion simulating disease1 (LSD1) and elongated hypocotyl 5 (HY5) perform opposite roles to regulate excess red light (RL)-triggered PCD associated with ROS and SA production. Under RL, the lsd1 mutant released more ROS and SA and displayed a stronger cell death rate than the hy5 mutant. It was shown that active LSD1 converted into inactive form by changing the redox status of the plastoquinone pool, and HY5 interacted with phytochrome B (phyB) to promote PCD in response to RL. LSD1 inhibited the enhanced disease susceptibility 1 (EDS1) expression by upregulating SR1, whereas HY5 enhanced the enhanced EDS1 expression by binding to the G-box of the EDS1 promoter. This study suggested that LSD1 and HY5 antagonistically modulated EDS1-dependent ROS and SA signaling; thus, PCD was mediated in response to RL.
Highlights
Programmed cell death (PCD) is involved in plant growth and development
The lsd1-2 mutant and WT treated with DCMU under ambient light for 4 h and exposed to Excess light (EL) or red light (RL) showed a significant decrease in PCD compared with that treated with RL alone; by contrast, the hy5-215 mutant leaves of the same treatment were slightly different (Figure 1)
The lsd1-2 mutant accumulates higher reactive oxygen species (ROS) and salicylic acid (SA) concentrations, whereas the hy5-215 mutant accumulates lower ROS and SA concentrations under RL; this result indicated that lesion simulating disease1 (LSD1) and hypocotyl 5 (HY5) play different roles in regulating ROS and SA signaling in response to RL (Figure 2)
Summary
Programmed cell death (PCD) is involved in plant growth and development. PCD is closely related to defense during plant–pathogen interactions or acclimation in response to abiotic stress (Rusterucci et al, 2001; Gechev et al, 2006). The onset of PCD in plants is dependent on light, which is essential to the life cycle of plants. Excess light (EL) stress triggers the release of reactive oxygen species (ROS) and subsequently induces PCD in plants; red light (RL) is vital in this process (Asada, 1999; Mateo et al, 2004). ROS, which often interacts with salicylic acid (SA) and ethylene (ET), contributes to the progress of light-dependent PCD (Mazel and Levine, 2001; Muhlenbock et al, 2008; Li et al, 2013). Phytochrome B (phyB) is a major RL photoreceptor that positively regulates ROS production and cell death during de-etiolation response (Nagatani, 2004; Chen et al, 2013)
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