Phloem loading in the sucrose-export-defective (SXD-1) mutant maize is limited by callose deposition at plasmodesmata in bundle sheath—vascular parenchyma interface

Botha, C. E. J.; Cross, R. H. M.; Bel, Aart J. E. van; Peter, Craig I.

doi:10.1007/bf02524263

Cited by 85 publications

(69 citation statements)

References 33 publications

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“…4). These effects concur well with the assumption that the blockage of the symplastic transport route into minor veins, as demonstrated previously by dye-coupling microinjection studies for sxd1 mutant leaves (Botha et al, 2000), would likewise affect carbon and nitrogen allocation. The increase of Pro contents in source leaves of phenotypic line StSXD1-RNAi-22, and less pronounced of line StSXD1-RNAi-27, further indicated an enhanced stress response as a consequence of tocopherol reduction and/or excess carbohydrate accumulation.…”

Section: Severe Tocopherol Deficiency Is Required To Induce a Blockagsupporting

confidence: 91%

“…The assimilate export-deficient phenotype in the maize sxd1 mutant has previously been attributed to callose occlusion of PD at the BS-VP interface of maturating leaf blades, thereby preventing the symplastic transport of Suc into the phloem tissue (Botha et al, 2000;Provencher et al, 2001). Therefore, callose concentration and distribution were analyzed in the same lower source leaves of tocopherol-deficient potato lines in comparison to wild type as used for photoassimilate determination before (leaf 11;compare Figs.…”

Section: Tocopherol Deficiency Causes Enhanced Callose Deposition In mentioning

confidence: 99%

“…This assumption was based on a typical photosynthate export-deficient phenotype characterized by an overall growth reduction and source leaf-specific accumulation of anthocyanins and starch. In addition, minor veins of maturating sxd1 leaf blades exhibited ultrastructural alterations and callose occlusion of a specific class of PD between bundle sheath (BS) and vascular parenchyma (VP) cells (Russin et al, 1996;Botha et al, 2000). This suggested an inhibition of symplastic continuity at the BS-VP boundary, leading to a block of Suc transport into the phloem.…”

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confidence: 99%

“…This suggested an inhibition of symplastic continuity at the BS-VP boundary, leading to a block of Suc transport into the phloem. Indeed, symplastic transport of the fluorescent dye Lucifer Yellow into minor veins was specifically blocked in anthocyaninaccumulating source regions of sxd1 leaf blades (Botha et al, 2000). Therefore, it was tempting to speculate that the respective mutation would reside in a gene that is essential for PD function.…”

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confidence: 99%

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RNAi-Mediated Tocopherol Deficiency Impairs Photoassimilate Export in Transgenic Potato Plants

et al. 2004

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Tocopherols (vitamin E) are lipophilic antioxidants presumed to play a key role in protecting chloroplast membranes and the photosynthetic apparatus from photooxidative damage. Additional nonantioxidant functions of tocopherols have been proposed after the recent finding that the Suc export defective1 maize (Zea mays) mutant (sxd1) carries a defect in tocopherol cyclase (TC) and thus is devoid of tocopherols. However, the corresponding vitamin E deficient1 Arabidopsis mutant (vte1) lacks a phenotype analogous to sxd1, suggesting differences in tocopherol function between C4 and C3 plants. Therefore, in this study, the potato (Solanum tuberosum) ortholog of SXD1 was isolated and functionally characterized. StSXD1 encoded a protein with high TC activity in vitro, and chloroplastic localization was demonstrated by transient expression of green fluorescent protein-tagged fusion constructs. RNAi-mediated silencing of StSXD1 in transgenic potato plants resulted in the disruption of TC activity and severe tocopherol deficiency similar to the orthologous sxd1 and vte1 mutants. The nearly complete absence of tocopherols caused a characteristic photoassimilate export-defective phenotype comparable to sxd1, which appeared to be a consequence of vascular-specific callose deposition observed in source leaves. CO 2 assimilation rates and photosynthetic gene expression were decreased in source leaves in close correlation with excess sugar accumulation, suggesting a carbohydrate-mediated feedback inhibition rather than a direct impact of tocopherol deficiency on photosynthetic capacity. This conclusion is further supported by an increased photosynthetic capacity of young leaves regardless of decreased tocopherol levels. Our data provide evidence that tocopherol deficiency leads to impaired photoassimilate export from source leaves in both monocot and dicot plant species and suggest significant differences among C3 plants in response to tocopherol reduction.

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Section: Severe Tocopherol Deficiency Is Required To Induce a Blockagsupporting

confidence: 91%

Section: Tocopherol Deficiency Causes Enhanced Callose Deposition In mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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RNAi-Mediated Tocopherol Deficiency Impairs Photoassimilate Export in Transgenic Potato Plants

et al. 2004

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“…sxd1 mutants show reduced Suc export capacity and accumulate large quantities of carbohydrates in the distal regions of leaf blades. An examination of the cellular interfaces in these distal regions revealed that callose is ectopically deposited over the cell wall between the bundle sheath and vascular parenchyma cells in leaf minor veins, thereby occluding the plasmodesmata (Botha et al, 2000). This defect is proposed to prevent Suc movement into the vascular parenchyma cells and result in the accumulation of carbohydrates in photosynthetic cells.…”

Section: Suc Entry Into a Veinmentioning

confidence: 99%