Abstract
Salinization of water and soil has a negative impact on tomato (Solanum lycopersicum L.) productivity by reducing growth of sink organs and by inducing senescence in source leaves. It has been hypothesized that yield stability implies the maintenance or increase of sink activity in the reproductive structures, thus contributing to the transport of assimilates from the source leaves through changes in sucrolytic enzymes and their regulation by phytohormones. In this study, classical and functional physiological approaches have been integrated to study the influence of metabolic and hormonal factors on tomato fruit sink activity, growth, and yield: (i) exogenous hormones were applied to plants, and (ii) transgenic plants overexpressing the cell wall invertase (cwInv) gene CIN1 in the fruits and de novo cytokinin (CK) biosynthesis gene IPT in the roots were constructed. Although salinity reduces fruit growth, sink activity, and trans-zeatin (tZ) concentrations, it increases the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) during the actively growing period (25 days after anthesis). Indeed, exogenous application of the CK analogue kinetin to salinized actively growing fruits recovered sucrolytic activities (mainly cwInv and sucrose synthase), sink strength, and fruit weight, whereas the ethylene-releasing compound ethephon had a negative effect in equivalent non-stressed fruits. Fruit yield was increased by both the constitutive expression of CIN1 in the fruits (up to 4-fold) or IPT in the root (up to 30%), owing to an increase in the fruit number (lower flower abortion) and in fruit weight. This is possibly related to a recovery of sink activity in reproductive tissues due to both (i) increase in sucrolytic activities (cwInv, sucrose synthase, and vacuolar and cytoplasmic invertases) and tZ concentration, and (ii) a decrease in the ACC levels and the activity of the invertase inhibitor. This study provides new functional evidences about the role of metabolic and hormonal inter-regulation of local sink processes in controlling tomato fruit sink activity, growth, and yield under salinity.
Highlights
Salinity decreases crop yield by first reducing growth and the number of assimilate-consuming sink organs, and by decreasing assimilate production in photosynthetically active source tissues (Hsiao, 1973; Cramer, 1992; Chazen et al, 1995)
Classical and functional physiological approaches have been integrated to study the influence of metabolic and hormonal factors on tomato fruit sink activity, growth, and yield: (i) exogenous hormones were applied to plants, and (ii) transgenic plants overexpressing the cell wall invertase gene CIN1 in the fruits and de novo cytokinin (CK) biosynthesis gene IPT in the roots were constructed
The result of multiplying sink activity by the sink size was considered as the fruit sink strength, expressed in Bq fruit–1
Summary
Salinity decreases crop yield by first reducing growth and the number of assimilate-consuming sink organs (both vegetative and reproductive), and by decreasing assimilate production in photosynthetically active source tissues (Hsiao, 1973; Cramer, 1992; Chazen et al, 1995). Decreased fruit set and/or tomato fruit weight and, crop yield under salinity conditions have been partially explained in terms of sucrose transport and metabolism (Ho, 1996) In this regard, it has been reported that a highly saline treatment (150 mM NaCl for 10 d) decreased pollen viability, inducing tomato flower abortion, which was thought to be due to decreased carbohydrate transport from source leaves to the inflorescence and pollen-producing tissues, as suggested by marked reductions in sucrolytic activities of cwInv and SUS (Ghanem et al, 2009). An inverse relationship between cytoplasmic sucrolytic activities (CSA) and cwInv in fruits of domestic and hybrid (between Solanum lycopersicum and the wild relatives S. cheesmaniae and S. chmielewskii) tomato plants has been reported as a regulatory mechanism for maintaining sink capacity and dry matter accumulation (Balibrea et al, 2003; Balibrea et al, 2006)
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