Light affects ascorbate content and ascorbate-related gene expression in tomato leaves more than in fruits

Abstract

Little is known about the light regulation of vitamin C synthesis in fruits. In contrast, previous studies in leaves revealed that VTC2 (coding for GDP-L: -galactose phosphorylase) was one of the key genes up-regulated by light in leaves. Our objective was to determine how the expression of ascorbate (AsA) synthesis genes in tomato (Solanum lycopersicum) was modified according to light irradiance in both leaves and fruits. Seven days of shading strongly decreased total ascorbate (reduced and oxidized form) content in leaves (50%) and to a lesser extent in fruits (10%). Among the last six steps of AsA biosynthesis, only two genes, VTC2 and GPP1 (one of the two unigenes coding for L: -galactose-1-P phosphatase in tomato), were down-regulated by long-term shading in red ripe fruits, compared to seven genes regulated in leaves. This underlines that light affects AsA-related gene expression more in leaves than in ripening fruits. Moreover, this study reveals strong daily changes in transcript levels of enzymes of the AsA biosynthetic pathway in leaves (11 of the 12 studied genes showed significant changes in their expression pattern). Among those genes, we found that diurnal variation in transcript levels of VTC2 and GME1 correlated to leaf AsA content measured 8 h later. This study provides a new hypothesis on the role of GME1 in addition to VTC2 in light-regulated AsA biosynthesis.

Ascorbate metabolism in vegetative and reproductive organs of "cherry" tomato

“…1). In accordance to our results, Massot et al (2012) reported almost two-fold difference in concentration of tAsA in leaves than in fruits of tomato. Our results revealed that the most active fruit tissue is the pericarp, where transcripts were, in most cases, almost twofold higher compared to the pulp.…”

“…In contrast, transcripts of most of the genes exhibited lower accumulation in fruits than in tissues with high photosynthetic potential as well as in roots. These results can be attributed into two factors; the differences in light effect in fruit and in organs with high photosynthetic potential (Massot et al 2012) and the different respira-tion rate between mature fruits and fast growing organs as flowers and root tips. Indeed, both factors are reported to have an effect on AsA metabolism (Bartoli et al 2006).…”

Investigating the role of vitamin C in tomato through TILLING identification of ascorbate-deficient tomato mutants

“…Three tomato genes were targeted: the SlGMP2 gene (SGN-U568548) encoding the GDP-d-mannose pyrophosphorylase (GMP), the SlGME1 (SGN-U581327) encoding the GDP-d-mannose epimerase and the SlGGP2 gene (SGN-U579800) encoding the GDP-l-galactose phosphorylase. Selection of the genes was done based on their expression patterns in the fruit, regulation by light (Massot et al 2012) and differential expression in a AsAdeficient GME-silenced tomato transgenic line ).…”

“…Same explanation may hold true for the GME1-5944 line, though the mild ascorbate phenotype observed in this line may also result from the creation of a weak allele by the missense mutation. More unexpected is that, despite the expression of two genes encoding GDP-l-galactose phosphorylase in tomato (Massot et al 2012), the two independent Slggp2 truncation and splice junction mutant lines have only ∼5% residual ascorbate content in the leaves (Figure 3). This result indicates that the two GGP genes found in tomato are not functionally redundant and are unable to complement each other in the conditions studied.…”

“…Interestingly, the Slgme1 mutant was able to withstand the stress imposed. Possible explanation is that the adaptation of Slgme1 mutant to high light intensity may result from the up-regulation of ascorbate biosynthesis genes in the leaf in response to light (Massot et al 2012) and therefore in ascorbate production. The up-regulation of either SlGME1 or SlGME2 and as a consequence of GME activity in the leaf would be sufficient to compensate for a weak missense mutation in SlGME1.…”