Nitrate-dependent shoot sodium accumulation and osmotic functions of sodium in Arabidopsis under saline conditions.

Improving crop plants to be productive in saline soils or under irrigation with saline water would be an important technological advance in overcoming the food and freshwater crises that threaten the world population. However, even if the transformation of a glycophyte into a plant that thrives under seawater irrigation was biologically feasible, current knowledge about Na+ effects would be insufficient to support this technical advance. Intriguingly, crucial details about Na+ uptake and its function in the plant have not yet been well established. We here propose that under saline conditions two nitrate-dependent transport systems in series that take up and load Na+ into the xylem constitute the major pathway for the accumulation of Na+ in Arabidopsis shoots; this pathway can also function with chloride at high concentrations. In nrt1.1 nitrate transport mutants, plant Na+ accumulation was partially defective, which suggests that NRT1.1 either partially mediates or modulates the nitrate-dependent Na+ transport. Arabidopsis plants exposed to an osmotic potential of -1.0 MPa (400 mOsm) for 24 h showed high water loss and wilting in sorbitol or Na/MES, where Na+ could not be accumulated. In contrast, in NaCl the plants that accumulated Na+ lost a low amount of water, and only suffered transitory wilting. We discuss that in Arabidopsis plants exposed to high NaCl concentrations, root Na+ uptake and tissue accumulation fulfil the primary function of osmotic adjustment, even if these processes lead to long-term toxicity.

Salt intolerance in Arabidopsis: shoot and root sodium toxicity, and inhibition by sodium-plus-potassium overaccumulation.

MAIN CONCLUSION: Arabidopsis plants in NaCl suffering half growth inhibition do not suffer osmotic stress and seldom shoot Na (+) toxicity; overaccumulation of Na (+) plus K (+) might trigger the inhibition. It is widely assumed that salinity inhibits plant growth by osmotic stress and shoot Na(+) toxicity. This study aims to examine the growth inhibition of Arabidopsis thaliana by NaCl concentrations that allow the completion of the life cycle. Unaffected Col-0 wild-type plants were used to define nontoxic Na(+) contents; Na(+) toxicities in shoots and roots were analyzed in hkt1 and sos1 mutants, respectively. The growth inhibition of Col-0 plants at 40 mM Na(+) was mild and equivalent to that produced by 8 and 4 mM Na(+) in hkt1 and sos1 plants, respectively. Therefore, these mutants allowed to study the toxicity of Na(+) in the absence of an osmotic challenge. Col-0 and Ts-1 accessions showed very different Na(+) contents but similar growth inhibitions; Ts-1 plants showed very high leaf Na(+) contents but no symptoms of Na(+) toxicity. Ak-1, C24, and Fei-0 plants were highly affected by NaCl showing evident symptoms of shoot Na(+) toxicity. Increasing K(+) in isotonic NaCl/KCl combinations dramatically decreased the Na(+) content in all Arabidopsis accessions and eliminated the signs of Na(+) toxicity in most of them but did not relieve growth inhibition. This suggested that the dominant inhibition in these conditions was either osmotic or of an ionic nature unspecific for Na(+) or K(+). Col-0 and Ts-1 plants growing in sorbitol showed a clear osmotic stress characterized by a notable decrease of their water content, but this response did not occur in NaCl. Overaccumulation of Na(+) plus K(+) might trigger growth reduction in NaCl-treated plants.

Sas3-mediated histone acetylation regulates effector gene activation in a fungal plant pathogen.

IMPORTANCE: Pathogen infections require the production of effectors that enable host colonization. Effectors have diverse functions and are only expressed at certain stages of the infection cycle. Thus, effector genes are tightly regulated by several mechanisms, including chromatin remodeling. Here, we investigate the role of histone acetylation in effector gene activation in the fungal wheat pathogen Zymoseptoria tritici. We demonstrate that lysine acetyltransferases (KATs) are essential for the spatiotemporal regulation of effector genes. We show that the KAT Sas3 is involved in leaf symptom development and pycnidia formation. Importantly, our results indicate that Sas3 controls histone acetylation of effector loci and is a regulator of effector gene activation during stomatal penetration. Overall, our work demonstrates the key role of histone acetylation in regulating gene expression associated with plant infection.