| Description: | Sugars such as glucose function as signal molecules that regulate gene expression, growth and development in plants, animals and yeast. To understand the molecular mechanisms of sugar responses, we isolated and characterized an Arabidopsis thaliana mutant, high sugar- response 8 (hsr8), which enhances sugar responsive growth and gene expression. Light- grown hsr8 plants exhibited increased starch and anthocyanin and reduced chlorophyll content in response to glucose treatment. Dark- grown hsr8 seedlings show glucose- hypersensitive hypocotyl elongation and development. The HSR8 gene, isolated using map-based cloning, is allelic to the MUR4 gene involved in arabinose synthesis. Dark- grown mur1 and mur3 seedlings also exhibit similar sugar responses to hsr8/mur4. The sugar- hypersensitive phenotypes of hsr8/mur4, mur1 and mur3 were restored to those of WT by boric acid, suggesting that alterations in the cell wall cause hypersensitive sugar- responsive phenotypes. Genetic analysis showed that sugar- hypersensitive responses in hsr8 mutants were suppressed by prl1, indicating that nuclear-localised PRL1 is required for enhanced sugar-responses in hsr8 mutant plants. Microarray analysis revealed that expression of many cell wall-related and sugar-responsive genes was altered in mur4-1, and expression of a significant proportion of these genes was restored to wild type levels in the mur4-1prl1 double mutant. These findings reveal a pathway that signals changes in the cell wall through PRL1 to altered gene expression and sugar- responsive metabolic, growth and developmental changes. The above experiments are conducted on 6d-old seedlings grown on medium containning 1% glucose in dark. |
NASCArrays Information at The BAR
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