As in metazoans, life in oxygenic photosynthetic organisms relies on the accurate regulation of cell death. During development and in response to the environment, photosynthetic cells activate and execute cell death pathways that culminate in the death of a specific group of cells, a process known as regulated cell death (RCD). RCD control is instrumental, as its mis regulation can lead to growth penalties and even the death of the entire organism. Intracellular molecules released during cell demise may act as “survival” or “death” signals and control the propagation of cell death to surrounding cells, even in unicellular organisms. This review explores different signals involved in cell-cell communication and systemic signaling in photosynthetic organisms, in particular Ca ²⁺, ROS, lipid derivates, NO and eATP. We discuss their possible mode-of-action as either “survival” and “death” molecules and their potential role in determining cell fate in neighboring cells. By comparing the knowledge available across the taxonomic spectrum of this coherent phylogenetic group, from cyanobacteria to vascular plants, we aim at contributing to the identification of conserved mechanisms that control cell death propagation in oxygenic photosynthetic organisms.

Aims: Nitrogen (N) is an essential nutrient for plant growth and seed production, being nitrate the main source of N in soils. Although several molecular players of plant responses to nitrate signaling were unraveled, it still remains a complex pathway with gaps demanding further investigation. The aim of our study is to analyze the role of Nitric Oxide (NO) in the Primary Nitrate Response (PNR). Results: Using a combination of genetic and pharmacological approaches, we demonstrate that NO is required for the expression of the nitrate-regulated genes NIA1, NIR, NRT1.1, and NRT2.1 in Arabidopsis. The PNR is blocked in the Arabidopsis mutant noa1, defective in NO production. Our results also show that Phytoglobin 1, involved in NO homeostasis, is rapidly induced during PNR in wt but not in mutants nrt1.1 and nlp7, suggesting that NRT1.1-NLP7 cascade modulates Phytoglobin expression. Biotin switch experiments demonstrate that NLP7, the PNR-master regulator, is S-nitrosated. NO appears to be not involved in the decrease of ROS concentration necessary for the PNR to take place, indicating that ROS and NO acts in independent ways. Besides, in the absence of NO, PNR does not occur even when the ROS concentration is low, indicating that the decrease in ROS concentration is a necessary but not sufficient condition for PNR to occur. Conclusion and Innovation: NO, a byproduct of nitrate metabolism and a well characterized signal molecule in plants, is a critical player in the PNR.

Introduction: Photosynthetic organisms respond to nitrogen (N) deprivation with the slowdown of photosynthesis and electron transport resulting in the balance the carbon (C)/N ratio. Under this extreme condition, organisms trigger complex mechanisms to keep growing using different N sources and recycling N containing molecules. In particular, phytoplankton are able to uptake L-arginine (L-Arg) as an organic N source. L-Arg can be assimilated mainly by the arginase, arginine deimidase, arginine decarboxylase or L-amino oxidase pathways.Results: We analyzed the effect of different N sources on the growth of the green algae Ostreococcus tauri. N starvation caused an inhibition of culture growth and a decrease in chlorophyll content. The addition of L-Arg to an N-deprived medium promotes a sustained growth rate of O. tauri culture and the increase of chlorophyll levels. The transcript level of genes involved in N uptake and metabolism were increased in N-starved condition while the addition of L-Arg as the sole N source reduced their induction. Since the O. tauri genome lacks the classical pathways to metabolize L-Arg, another enzyme/s may be responsible for L-Arg catabolism. Previously, we characterized the nitric oxide synthase (NOS) enzyme from O. tauri (OtNOS) which oxidizes L-Arg producing nitric oxide (NO) and citrulline. The NOS inhibitor L-NAME blocks the effect promoted by L-Arg on N-deprived O. tauri growth. Besides, NO level increased in O. tauri cells growing in L-Arg containing medium, suggesting the participation of OtNOS enzyme in L-Arg metabolism during N starvation.Discussion: Our hypothesis suggests that, after NOS-dependent Arg degradation, non-enzymatic oxidation of NO produces N oxides (mainly NO₂^-) that are re-incorporated to the N primary metabolism. As expected, N deprivation increases the lipid content in Ostreococcus. The addition of L-Arg or NO₂^- as the sole N sources showed a similar increase in lipid content to N deprivation. In summary, our results demonstrate that L-Arg is able to function as N source in Ostreococcus. The evidences on an alternative pathway of N supply and metabolism in a photosynthetic microorganism are discussed. These results could also allow the development of biotechnological tools for increasing lipid production for industry.