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Peer-reviewedCC BY 4.0Plant Physiology

Tissue-specific accumulation of Na+ in leaves of 2 tomato species is linked to differences in symplastic transport

Abstract

Soil salinization is a growing global threat that limits crop productivity. To cope with sodium (Na+) stress, plants have evolved tolerance mechanisms, including excluding Na+ from shoot tissues and tolerating elevated Na+ within shoots through tissue- and cellular-level mechanisms. Most current knowledge of Na+ accumulation comes from organ- or whole-plant measurements that lack the spatial resolution needed to resolve cellular tolerance mechanisms. Here, we used histological approaches to map leaf Na+ distribution in tomato (Solanum) species with contrasting salt-tolerance strategies. In the moderately salt-tolerant, Na+-excluding domesticated tomato (cv. M82), Na+ was largely confined to the bundle sheath, whereas in salt-tolerant, Na+-including wild relatives, Na+ accumulated throughout the blade mesophyll. Consistent with these cell population-specific Na+ patterns, M82, but not Solanum pennellii, exhibited reduced symplastic transport and plasmodesma permeability under salt stress. A genetic screen combined with transcriptome profiling implicated Plasmodesmata-Located Protein 1 (PDLP1), a regulator of callose-mediated plasmodesma closure, in establishing symplastic domains in M82 that restrict Na+ movement into the mesophyll. Moreover, PDLP1 expression was negatively correlated with mesophyll Na+ levels across wild and domesticated tomatoes. Collectively, these results link cellular Na+ enrichment patterns to symplastic connectivity and suggest that PDLP1-mediated regulation of plasmodesmata contributes to leaf-level salt-tolerance strategies.

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BibTeX
@article{shaarmoshe2026tissuespecific,
  title = {{Tissue-specific accumulation of Na+ in leaves of 2 tomato species is linked to differences in symplastic transport}},
  author = {Lidor Shaar-Moshe and Daniel E Runcie and Siobhán M Brady},
  journal = {Plant Physiology},
  year = {2026},
  month = nov,
  doi = {10.1093/plphys/kiag779},
  url = {https://doi.org/10.1093/plphys/kiag779},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Tissue-specific accumulation of Na+ in leaves of 2 tomato species is linked to differences in symplastic transport
AU  - Lidor Shaar-Moshe
AU  - Daniel E Runcie
AU  - Siobhán M Brady
PY  - 2026
DA  - 2026/11/04
JO  - Plant Physiology
DO  - 10.1093/plphys/kiag779
UR  - https://doi.org/10.1093/plphys/kiag779
AB  - Soil salinization is a growing global threat that limits crop productivity. To cope with sodium (Na+) stress, plants have evolved tolerance mechanisms, including excluding Na+ from shoot tissues and tolerating elevated Na+ within shoots through tissue- and cellular-level mechanisms. Most current knowledge of Na+ accumulation comes from organ- or whole-plant measurements that lack the spatial resolution needed to resolve cellular tolerance mechanisms. Here, we used histological approaches to map leaf Na+ distribution in tomato (Solanum) species with contrasting salt-tolerance strategies. In the moderately salt-tolerant, Na+-excluding domesticated tomato (cv. M82), Na+ was largely confined to the bundle sheath, whereas in salt-tolerant, Na+-including wild relatives, Na+ accumulated throughout the blade mesophyll. Consistent with these cell population-specific Na+ patterns, M82, but not Solanum pennellii, exhibited reduced symplastic transport and plasmodesma permeability under salt stress. A genetic screen combined with transcriptome profiling implicated Plasmodesmata-Located Protein 1 (PDLP1), a regulator of callose-mediated plasmodesma closure, in establishing symplastic domains in M82 that restrict Na+ movement into the mesophyll. Moreover, PDLP1 expression was negatively correlated with mesophyll Na+ levels across wild and domesticated tomatoes. Collectively, these results link cellular Na+ enrichment patterns to symplastic connectivity and suggest that PDLP1-mediated regulation of plasmodesmata contributes to leaf-level salt-tolerance strategies.
SN  - 0032-0889
SN  - 1532-2548
ER  -