Salinity Effects on Sugar Homeostasis and Vascular Anatomy in the Stem of the Arabidopsis Thaliana Inflorescence.

The regulation of sugar metabolism and partitioning plays an essential role for a plant's acclimation to its environment, with specific responses in autotrophic and heterotrophic organs. In this work, we analyzed the effects of high salinity on sugar partitioning and vascular anatomy within the floral stem. Stem sucrose and fructose content increased, while starch reduced, in contrast to the response observed in rosette leaves of the same plants. In the stem, the effects were associated with changes in the expression of SWEET and TMT2 genes encoding sugar transporters, SUSY1 encoding a sucrose synthase and several FRK encoding fructokinases. By contrast, the expression of SUC2, SWEET11 and SWEET12, encoding sugar transporters for phloem loading, remained unchanged in the stem. Both the anatomy of vascular tissues and the composition of xylem secondary cell walls were altered, suggesting that high salinity triggered major readjustments of sugar partitioning in this heterotrophic organ. There were changes in the composition of xylem cell walls, associated with the collapse and deformation of xylem vessels. The data are discussed regarding sugar partitioning and homeostasis of sugars in the vascular tissues of the stem.

Arabidopsis Natural Accessions Display Adaptations in Inflorescence Growth and Vascular Anatomy to Withstand High Salinity during Reproductive Growth.

Plant responses to abiotic stresses entail adaptive processes that integrate both physiological and developmental cues. However, the adaptive traits that are involved in the responses to a high soil salinity during reproductive growth are still poorly studied. To identify new clues, we studied the halophyte, Thellungiella salsuginea, and three Arabidopsis accessions, known as tolerant or salt-sensitive. We focused on the quantitative traits associated with the stem growth, sugar content, and anatomy of the plants subjected to the salt treatment, with and without a three-day acclimation, applied during the reproductive stage. The stem growth of Thellungiella salsuginea was not affected by the salt stress. By contrast, salt affected all of the Arabidopsis accessions, with a natural variation in the effect of the salt on growth, sugar content, and stem anatomy. In response to the high salinity, irregular xylem vessels were observed, independently of the accession's tolerance to salt treatment, while the diameter of the largest xylem vessels was reduced in the tolerant accessions. The stem height, growth rate, hexoses-to-sucrose ratio, and phloem-to-xylem ratio also varied, in association with both the genotype and its tolerance to salt stress. Our findings indicate that several quantitative traits for salt tolerance are associated with the control of inflorescence growth and the adjustment of the phloem-to-xylem ratio.

The Lmpma1 gene of Leptosphaeria maculans encodes a plasma membrane H+-ATPase isoform essential for pathogenicity towards oilseed rape.

Following Agrobacterium tumefaciens-mediated mutagenesis in Leptosphaeria maculans, we identified the mutant 210, displaying total loss of pathogenicity towards its host plant (Brassica napus). Microscopic observations showed that m210 is unable to germinate on the host leaf surface and is thus blocked at the pre-penetration stage. The pathogenicity phenotype is linked with a single T-DNA insertion into the promoter region of a typical plasma membrane H(+)-ATPase-encoding gene, termed Lmpma1, thus leading to a twofold reduction in Lmpma1 expression. Since LmPMA1 is involved in intracellular pH homeostasis, we postulate that reduction in LmPMA1 activity disturbs the electrochemical transmembrane gradient in m210, thus leading to conidia defective in turgor pressure generation on leaf surface. Whole genome survey showed that L. maculans possesses a second plasma membrane H(+)-ATPase-encoding gene, termed Lmpma2. Silencing experiments, expression analyses and phylogenetic studies allowed us to highlight the essential role assumed by the Lmpma1 isoform in L.maculans pathogenicity.