title: The HAL1 function on Na+ homeostasis is maintained over time in salt-treated transgenic tomato plants, but the high reduction of Na+ in leaf is not associated with salt tolerance.
abstract: To achieve a deeper knowledge on the function of HAL1 gene in tomato (Solanum lycopersicum) plants submitted to salt stress, in this study, we studied the growth and physiological responses to high salt stress of T3 transgenic plants (an azygous line without transgene and both homozygous and hemizygous lines for HAL1) proceeding from a primary transformant with a very high expression level of HAL1 gene. The homozygous plants for HAL1 gene did not increase their salt tolerance in spite of an earlier and higher reduction of the Na(+) accumulation in leaves, being moreover the Na(+) homeostasis maintained throughout the growth cycle. The greater ability of the homozygous line to regulate the Na(+) transport to the shoot to long term was even shown in low accumulation of Na(+) in fruits. By comparing the homozygous and hemizygous lines, a higher salt tolerance in the hemizygous line, with respect to the homozygous line, was observed on the basis of fruit yield. The Na(+) homeostasis and osmotic homeostasis were also different in homozygous and hemizygous lines. Indeed, the Na(+) accumulation rate in leaves was greater in hemizygous than in homozygous line after 35 days of 100 mM NaCl treatment and only at the end of growth cycle did the hemizygous line show leaf Na(+) levels similar to those found in the homozygous line. With respect to the osmotic homeostasis, the main difference between lines was the different contribution of inorganic and organic solutes to the leaf osmotic balance. Taken together, these results suggest that the greater Na(+) exclusion ability of the homozygous line overexpressing HAL1 induces a greater use of organic solutes for osmotic balance, which seems to have an energy cost and hence a growth penalty that reverts negatively on fruit yield.
authors.affiliation: Department of Stress Biology and Plant Pathology, Centro de Edafología y Biología Aplicada del Segura (CSIC), Campus de Espinardo, Apdo 164, 30100-Espinardo, Murcia, Spain.
authors.forename: Alicia
authors.initials: A
authors.lastname: Muñoz-Mayor
authors.forename: Benito
authors.initials: B
authors.lastname: Pineda
authors.forename: Jose O
authors.initials: JO
authors.lastname: Garcia-Abellán
authors.forename: Begoña
authors.initials: B
authors.lastname: Garcia-Sogo
authors.forename: Elena
authors.initials: E
authors.lastname: Moyano
authors.forename: Alejandro
authors.initials: A
authors.lastname: Atares
authors.forename: Francisco
authors.initials: F
authors.lastname: Vicente-Agulló
authors.forename: Ramon
authors.initials: R
authors.lastname: Serrano
authors.forename: Vicente
authors.initials: V
authors.lastname: Moreno
authors.forename: Maria C
authors.initials: MC
authors.lastname: Bolarin
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects*; D050260:Carbohydrate Metabolism / Q000187:drug effects; D005638:Fruit / Q000187:drug effects / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects*; D006720:Homozygote; D047908:Intracellular Signaling Peptides and Proteins; D018551:Solanum lycopersicum / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development; D018515:Plant Leaves / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D010940:Plant Proteins / Q000378:metabolism; D018517:Plant Roots / Q000187:drug effects / Q000378:metabolism; D030821:Plants, Genetically Modified; D011188:Potassium / Q000494:pharmacology; D029701:Saccharomyces cerevisiae Proteins / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism* / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology*; D013997:Time Factors; D019076:Transgenes
chemical_list: C076232:HAL1 protein, S cerevisiae; D047908:Intracellular Signaling Peptides and Proteins; D010940:Plant Proteins; D029701:Saccharomyces cerevisiae Proteins; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium