Plants interact with the environment by sensing “non-self” molecules called elicitors derived from pathogens or other sources. These molecules bind to specific receptors located in the plasma membrane and trigger defense responses leading to protection against pathogens. In particular, it has been shown that cell wall and storage polysaccharides from green, brown and red seaweeds (marine macroalgae) corresponding to ulvans, alginates, fucans, laminarin and carrageenans can trigger defense responses in plants enhancing protection against pathogens. In addition, oligosaccharides obtained by depolymerization of seaweed polysaccharides also induce protection against viral, fungal and bacterial infections in plants. In particular, most seaweed polysaccharides and derived oligosaccharides trigger an initial oxidative burst at local level and the activation of salicylic (SA), jasmonic acid (JA) and/or ethylene signaling pathways at systemic level. The activation of these signaling pathways leads to an increased expression of genes encoding: (i) Pathogenesis-Related (PR) proteins with antifungal and antibacterial activities; (ii) defense enzymes such as pheylalanine ammonia lyase (PAL) and lipoxygenase (LOX) which determine accumulation of phenylpropanoid compounds (PPCs) and oxylipins with antiviral, antifugal and antibacterial activities and iii) enzymes involved in synthesis of terpenes, terpenoids and/or alkaloids having antimicrobial activities. Thus, seaweed polysaccharides and their derived oligosaccharides induced the accumulation of proteins and compounds with antimicrobial activities that determine, at least in part, the enhanced protection against pathogens in plants.

Enteromorpha compressa is the dominant species in coastal areas of northern Chile receiving copper mine wastes. Copper remains as the main heavy metal in these coastal waters and it is accumulated in E. compressa growing at the impacted sites. Algae from these sites showed higher levels of lipoperoxides than from non-impacted sites, which suggests the occurrence of cellular damage resulting from oxidative stress. The strong activation of ascorbate peroxidase detected in this study probably occurs in order to buffer this oxidative stress. Unexpectedly, the activity of glutathione reductase, normally coupled to ascorbate peroxidase activity, was not affected by the chronic exposure to the mine wastes. Moreover, catalase, dehydroascorbate reductase and glutathione peroxidase, commonly reported to buffer oxidative stress in plants and algae, were not detected in E. compressa from any of the studied sites. Levels of total glutathione and phenolic compounds decreased in algae from mine-impacted sites. In contrast, high levels of dehydroascorbate were found in algae from impacted sites, whereas ascorbate remained unchanged. Therefore, it is suggested that E. compressa tolerates a copper-enriched environment, and the accompanying oxidative stress, through the accumulation of copper, activation of ascorbate peroxidase, synthesis of ascorbate (accumulated as dehydroascorbate) and consumption of glutathione and water-soluble phenolic compounds.

To analyze the copper-induced cross talk among calcium, nitric oxide (NO), and hydrogen peroxide (H2O2) and the calcium-dependent activation of gene expression, the marine alga Ulva compressa was treated with the inhibitors of calcium channels, ned-19, ryanodine, and xestospongin C, of chloroplasts and mitochondrial electron transport chains, 3-(3,4-dichlorophenyl)-1,1-dimethylurea and antimycin A, of pyruvate dehydrogenase, moniliformin, of calmodulins, N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide, and of calcium-dependent protein kinases, staurosporine, as well as with the scavengers of NO, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, and of H2O2, ascorbate, and exposed to a sublethal concentration of copper (10 μm) for 24 h. The level of NO increased at 2 and 12 h. The first peak was inhibited by ned-19 and 3-(2,3-dichlorophenyl)-1,1-dimethylurea and the second peak by ned-19 and antimycin A, indicating that NO synthesis is dependent on calcium release and occurs in organelles. The level of H2O2 increased at 2, 3, and 12 h and was inhibited by ned-19, ryanodine, xestospongin C, and moniliformin, indicating that H2O2 accumulation is dependent on calcium release and Krebs cycle activity. In addition, pyruvate dehydrogenase, 2-oxoxglutarate dehydrogenase, and isocitrate dehydrogenase activities of the Krebs cycle increased at 2, 3, 12, and/or 14 h, and these increases were inhibited in vitro by EGTA, a calcium chelating agent. Calcium release at 2, 3, and 12 h was inhibited by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide and ascorbate, indicating activation by NO and H2O2. In addition, the level of antioxidant protein gene transcripts decreased with N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide and staurosporine. Thus, there is a copper-induced cross talk among calcium, H2O2, and NO and a calcium-dependent activation of gene expression involving calmodulins and calcium-dependent protein kinases.

Unlike the majority of genes encoding small nuclear RNAs, which are transcribed by RNA polymerase B, the U6 gene contains features found in both class B and class C genes, indicating the involvement of a combination of transcription factors normally specific to each class of genes. We present direct genetic and biochemical evidence that the U6 gene of Saccharomyces cerevisiae is transcribed by RNA polymerase C in vivo as well as in vitro. A mutant strain with a temperature‐sensitive defect in the large subunit of RNA polymerase C that results in defective transcription of tRNA and 5S RNA genes shows a corresponding defect in U6 RNA levels. Also, purified RNA polymerase C transcribes the U6 gene when supplemented with partially purified TFIIIB. The other class C transcription factors, TFIIIA and Tau (TFIIIC), are not required in this system.

It is now well established that plant cell wall oligosaccharides can stimulate or inhibit growth and development in plants. In addition, it has been determined that seaweed (marine algae) cell wall polysaccharides and derived oligosaccharides can enhance growth in plants. In particular, oligo-alginates obtained by depolymerization of alginates from brown seaweeds increase growth of different plants by enhancing nitrogen assimilation and basal metabolism. Interestingly, oligo-alginates also stimulate growth of marine and fresh water green microalgae, increasing the content of fatty acids. On the other hand, oligo-carrageenans obtained by depolymerization of carrageenans from red seaweeds increase growth of tobacco plants by enhancing photosynthesis, nitrogen assimilation, basal metabolism, and cell division. In addition, oligocarrageenans increase protection against viral, fungal, and bacterial infections in tobacco plants, which is determined, at least in part, by the accumulation of several phenylpropanoid compounds (PPCs) with antimicrobial activity. Moreover, oligo-carrageenans stimulate growth of 3-yearold Eucalyptus globulus trees by increasing photosynthesis, nitrogen assimilation, and basal metabolism. Furthermore, oligo-carrageenans induce an increase in cellulose content and in the level of essential oil and some PPCs with antimicrobial activities, suggesting that defense against pathogens may be also enhanced. Thus, seaweed oligosaccharides induce a dual beneficial effect in plants and trees, enhancing growth, which is determined by the increase in carbon and nitrogen assimilation, basal metabolism, and cell division, and defense against pathogens, which is determined by the accumulation of compounds with antimicrobial activities. In this sense, molecular mechanisms that potentially interconnect activation of plant growth and defense responses are discussed.