Root cultures of potato mutant lacking MSPI isoform, indispensable for photosynthetic light reactions, exhibit characteristics similar to intact plant roots
Language English Country Germany Media print-electronic
Document type Journal Article
PubMed
31887556
DOI
10.1016/j.jplph.2019.153091
PII: S0176-1617(19)30220-2
Knihovny.cz E-resources
- Keywords
- Carbohydrate allocation, In vitro cultivation, PsbO1 gene, Root branching,
- MeSH
- Alleles MeSH
- Photosynthesis genetics radiation effects MeSH
- Photosystem II Protein Complex genetics metabolism MeSH
- Plant Tubers genetics growth & development MeSH
- Plant Roots growth & development metabolism MeSH
- Cells, Cultured MeSH
- Manganese metabolism MeSH
- Carbohydrate Metabolism genetics MeSH
- Mutation MeSH
- Mutant Proteins chemistry genetics metabolism MeSH
- Protein Isoforms genetics metabolism MeSH
- Gene Expression Regulation, Plant genetics physiology MeSH
- Plant Proteins genetics metabolism MeSH
- Sucrose metabolism MeSH
- Solanum tuberosum genetics growth & development MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Photosystem II Protein Complex MeSH
- Manganese MeSH
- Mutant Proteins MeSH
- Protein Isoforms MeSH
- Plant Proteins MeSH
- Sucrose MeSH
Potato (Solanum tuberosum) mutant (ST) lacking one isoform of manganese-stabilizing protein (MSPI) of photosystem II exhibited besides spontaneous tuberization also growth changes with strongly impaired root system development. Previous studies revealed marked changes in carbohydrate levels and allocation within ST plant body. To verify causal relationship between changed carbohydrate balance and root growth restriction we engaged dark grown sucrose-supplied root organ-cultures of ST plants to exclude/confirm shoot effects. Unexpectedly, in ST root cultures we observed large alterations in growth and architecture as well as saccharide status similar to those found in the intact plant roots. The gene expression analysis, however, proved PsbO1 transcript (coding MSPI protein) neither in ST nor in WT root-organ cultures. Therefore, the results point to indirect effects of PsbO1 allele absence connected possibly with some epigenetic modulations.
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