Tanned or Sunburned: How Excessive Light Triggers Plant Cell Death.

Plants often encounter light intensities exceeding the capacity of photosynthesis (excessive light) mainly due to biotic and abiotic factors, which lower CO2 fixation and reduce light energy sinks. Under excessive light, the photosynthetic electron transport chain generates damaging molecules, hence leading to photooxidative stress and eventually to cell death. In this review, we summarize the mechanisms linking the excessive absorption of light energy in chloroplasts to programmed cell death in plant leaves. We highlight the importance of reactive carbonyl species generated by lipid photooxidation, their detoxification, and the integrating role of the endoplasmic reticulum in the adoption of phototolerance or cell-death pathways. Finally, we invite the scientific community to standardize the conditions of excessive light treatments.

Endoplasmic reticulum-mediated unfolded protein response is an integral part of singlet oxygen signalling in plants.

Singlet oxygen (1 O2 ) is a by-product of photosynthesis that triggers a signalling pathway leading to stress acclimation or to cell death. By analyzing gene expressions in a 1 O2 -overproducing Arabidopsis mutant (ch1) under different light regimes, we show here that the 1 O2 signalling pathway involves the endoplasmic reticulum (ER)-mediated unfolded protein response (UPR). ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60, and low concentrations of the UPR-inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1 O2 levels. Exposure of ch1 to high light stress ultimately leading to cell death resulted in a marked upregulation of the two UPR branches (bZIP60/IRE1 and bZIP28/bZIP17). Accordingly, mutational suppression of bZIP60 and bZIP28 increased plant phototolerance, and a strong UPR activation by high tunicamycin concentrations promoted high light-induced cell death. Conversely, light acclimation of ch1 to 1 O2 stress put a limitation in the high light-induced expression of UPR genes, except for the gene encoding the BIP3 chaperone, which was selectively upregulated. BIP3 deletion enhanced Arabidopsis photosensitivity while plants treated with a chemical chaperone exhibited enhanced phototolerance. In conclusion, 1 O2 induces the ER-mediated UPR response that fulfils a dual role in high light stress: a moderate UPR, with selective induction of BIP3, is part of the acclimatory response to 1 O2 , and a strong activation of the whole UPR is associated with cell death.

OXI1 and DAD Regulate Light-Induced Cell Death Antagonistically through Jasmonate and Salicylate Levels.

Singlet oxygen produced from triplet excited chlorophylls in photosynthesis is a signal molecule that can induce programmed cell death (PCD) through the action of the OXIDATIVE STRESS INDUCIBLE 1 (OXI1) kinase. Here, we identify two negative regulators of light-induced PCD that modulate OXI1 expression: DAD1 and DAD2, homologs of the human antiapoptotic protein DEFENDER AGAINST CELL DEATH. Overexpressing OXI1 in Arabidopsis (Arabidopsis thaliana) increased plant sensitivity to high light and induced early senescence of mature leaves. Both phenomena rely on a marked accumulation of jasmonate and salicylate. DAD1 or DAD2 overexpression decreased OXI1 expression, jasmonate levels, and sensitivity to photooxidative stress. Knock-out mutants of DAD1 or DAD2 exhibited the opposite responses. Exogenous applications of jasmonate upregulated salicylate biosynthesis genes and caused leaf damage in wild-type plants but not in the salicylate biosynthesis mutant Salicylic acid induction-deficient2, indicating that salicylate plays a crucial role in PCD downstream of jasmonate. Treating plants with salicylate upregulated the DAD genes and downregulated OXI1 We conclude that OXI1 and DAD are antagonistic regulators of cell death through modulating jasmonate and salicylate levels. High light-induced PCD thus results from a tight control of the relative activities of these regulating proteins, with DAD exerting a negative feedback control on OXI1 expression.

Influence of bacteria on the response of microalgae to contaminant mixtures.

When microalgae are exposed to contaminants, the role of associated bacteria within the phycosphere, the microenvironment surrounding algal cells, remains largely unknown. The present study investigated the importance of algae-associated bacteria on the responses of microalgae growth to metallic and organic toxicant exposure. The effects of a polluted sediment elutriate, and of metal or pesticide mixtures at environmentally relevant concentrations (<10 µg L-1) were assessed on the growth of two microalgae strains: Isochrysis galbana, a prymnesiophyte, and Thalassiosira delicatula, a centric diatom. Both cultures were maintained as axenic or bacterized under similar conditions in batch cultures. In axenic conditions, the metal mixture addition at low concentrations alleviated limitation of growth by metals for T. delicatula relative to control, but inhibited I. galbana growth at highest concentration. In similar axenic conditions, both T. delicatula and I. galbana growth were negatively inhibited by pesticide mixture at concentrations as low as 10 ng L-1. The bacterial diversities associated with the two microalgae strains were significantly different (Bray-Curtis dissimilarity greater than 0.9) but their impact on microalgae growth was similar. The presence of bacteria reduced algal growth rate by ca. 50% compared to axenic cultures, whereas no significant effect of sediment elutriate, metal or pesticide mixtures was noticed on non-axenic algal growth rates. These results show that bacteria may have a negative effect on algal growth but can reduce pesticide toxicity or metal availability to algae.