Source-to-sink transport of sugar is one of the major determinants of plant growth and relies on the efficient and controlled distribution of sucrose (and some other sugars such as raffinose and polyols) across plant organs through the phloem. However, sugar transport through the phloem can be affected by many environmental factors that alter source/sink relationships. In this paper, we summarize current knowledge about the phloem transport mechanisms and review the effects of several abiotic (water and salt stress, mineral deficiency, CO2, light, temperature, air, and soil pollutants) and biotic (mutualistic and pathogenic microbes, viruses, aphids, and parasitic plants) factors. Concerning abiotic constraints, alteration of the distribution of sugar among sinks is often reported, with some sinks as roots favored in case of mineral deficiency. Many of these constraints impair the transport function of the phloem but the exact mechanisms are far from being completely known. Phloem integrity can be disrupted (e.g., by callose deposition) and under certain conditions, phloem transport is affected, earlier than photosynthesis. Photosynthesis inhibition could result from the increase in sugar concentration due to phloem transport decrease. Biotic interactions (aphids, fungi, viruses…) also affect crop plant productivity. Recent breakthroughs have identified some of the sugar transporters involved in these interactions on the host and pathogen sides. The different data are discussed in relation to the phloem transport pathways. When possible, the link with current knowledge on the pathways at the molecular level will be highlighted.

Although leaf senescence results in a loss of photosynthetic carbon fixation, the senescence-dependent release of nutrients, especially of nitrogen, is important for the growth of young leaves and for reproduction. Environmental regulation of senescence is therefore a vital factor in the carbon and nitrogen economy of plants. Leaf senescence is a highly plastic trait that is affected by a range of different environmental factors including light, nutrient supply, CO2 concentration, and abiotic and biotic stress. In this review, the focus is on the impact of environmental conditions on sugar accumulation and sugar signalling during senescence. By signalling a high availability of carbon relative to nitrogen in the old leaves, sugar accumulation can trigger leaf senescence. Sugar-induced senescence is therefore particularly important under low nitrogen availability and may also play a role in light signalling. Whether or not sugars are involved in regulating the senescence response of plants to elevated CO2 remains unresolved. Senescence can be delayed or accelerated in elevated CO2 and no clear relationship between sugar accumulation and senescence has been found. Plasticity in the response to environmental factors, such as daylength and sugar accumulation, varies between different Arabidopsis accessions. This natural variation can be exploited to analyse the genetic basis of the regulation of senescence and the consequences for growth and fecundity. Different evolutionary strategies, i.e. early senescence combined with a high reproductive effort or late senescence combined with a low reproductive effort, may be an important adaptation of Arabidopsis accessions to their natural habitat.

There has been some debate whether leaf senescence is induced by sugar starvation or by sugar accumulation. External supply of sugars has been shown to induce symptoms of senescence such as leaf yellowing. However, it was so far not clear if sugars have a signalling function during developmental senescence. Glucose and fructose accumulate strongly during senescence in Arabidopsis thaliana (L.) Heynh. leaves. Using Affymetrix GeneChip analysis we determined the effect of sugar-induced senescence on gene expression. Growth on glucose in combination with low nitrogen supply induced leaf yellowing and changes in gene expression that are characteristic of developmental senescence. Most importantly, the senescence-specific gene SAG12, which was previously thought to be sugar-repressible, was induced over 900-fold by glucose. Induction of SAG12, which is expressed during late senescence, demonstrates that processes characteristic for late stages are sugar-inducible. Two MYB transcription factor genes, PAP1 and PAP2, were identified as senescence-associated genes that are induced by glucose. Moreover, growth on glucose induced genes for nitrogen remobilisation that are typically enhanced during developmental senescence, including the glutamine synthetase gene GLN1;4 and the nitrate transporter gene AtNRT2.5. In contrast to wild-type plants, the hexokinase-1 mutant gin2-1 did not accumulate hexoses and senescence was delayed. Induction of senescence by externally supplied glucose was partially abolished in gin2-1, indicating that delayed senescence was a consequence of decreased sugar sensitivity. Taken together, our results show that Arabidopsis leaf senescence is induced rather than repressed by sugars.

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