UV-Induced cell death in plants

Abstract

Plants are photosynthetic organisms that depend on sunlight for energy. Plants respond to light through different photoreceptors and show photomorphogenic development. Apart from Photosynthetically Active Radiation (PAR; 400-700 nm), plants are exposed to UV light, which is comprised of UV-C (below 280 nm), UV-B (280-320 nm) and UV-A (320-390 nm). The atmospheric ozone layer protects UV-C radiation from reaching earth while the UVR8 protein acts as a receptor for UV-B radiation. Low levels of UV-B exposure initiate signaling through UVR8 and induce secondary metabolite genes involved in protection against UV while higher dosages are very detrimental to plants. It has also been reported that genes involved in MAPK cascade help the plant in providing tolerance against UV radiation. The important targets of UV radiation in plant cells are DNA, lipids and proteins and also vital processes such as photosynthesis. Recent studies showed that, in response to UV radiation, mitochondria and chloroplasts produce a reactive oxygen species (ROS). Arabidopsis metacaspase-8 (AtMC8) is induced in response to oxidative stress caused by ROS, which acts downstream of the radical induced cell death (AtRCD1) gene making plants vulnerable to cell death. The studies on salicylic and jasmonic acid signaling mutants revealed that SA and JA regulate the ROS level and antagonize ROS mediated cell death. Recently, molecular studies have revealed genes involved in response to UV exposure, with respect to programmed cell death (PCD).

Figure 1

Low-fluence UV radiation activates UVR8 dependent photomorphogenesis. A, Increased level of UV-absorbing sunscreens gives acclimation response; B, Increased anti-oxidative proteins can act as ROS scavengers; C, Increased level of DNA repair enzymes can act on CPDs and 6-6 PPs lesions and may result in cell cycle arrest and overall growth inhibition.

Figure 2

High-fluence UV radiation activates UVR8 independent stress pathway and cell death. A, Stress from UV exposure activates the mitogen-activated protein kinases (MAPK) cascade which leads to regulation of PCD; B, ROS released from chloroplast and mitochondria causes membrane lipid and protein oxidation, Mitochondrial Transmembrane Potential (MTP) loss from mitochondria results in cytochrome c release and activation of caspases and finally DNA laddering; C, High UV stress leads to A and B, which result in cell shrinkage, nuclear condensation showing Apoptotic like-PCD (AL-PCD). * Dotted arrow indicates the stress response pathway activated by yet unknown UV photoreceptor; “?” indicates the unknown UV photoreceptor, obscure role of UVR8 dependant pathway under stress conditions and the mechanistic involvement of AtDAD1, AtDAD2 and AtBI in UV induced PCD is unclear.