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Role of callose synthases in transfer cell wall development in tocopherol deficient Arabidopsis mutants.

Maeda H, Song W, Sage T, Dellapenna D - Front Plant Sci (2014)

Bottom Line: However, introduction of gsl4 or gsl11 mutations individually into the vte2 background did not suppress callose deposition or the overall LT-induced phenotypes of vte2.Intriguingly, introduction of a mutation disrupting GSL5, the major GSL responsible for pathogen-induced callose deposition, into vte2 substantially reduced vascular callose deposition at LT, but again had no effect on the photoassimilate export phenotype of LT-treated vte2.These results suggest that GSL5 plays a major role in TCW callose deposition in LT-treated vte2 but that this GSL5-dependent callose deposition is not the primary cause of the impaired photoassimilate export phenotype.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Michigan State University East Lansing, MI, USA ; Cell and Molecular Biology Program, Michigan State University East Lansing, MI, USA ; Department of Botany, University of Wisconsin-Madison Madison, WI, USA.

ABSTRACT
Tocopherols (vitamin E) are lipid-soluble antioxidants produced by all plants and algae, and many cyanobacteria, yet their functions in these photosynthetic organisms are still not fully understood. We have previously reported that the vitamin E deficient 2 (vte2) mutant of Arabidopsis thaliana is sensitive to low temperature (LT) due to impaired transfer cell wall (TCW) development and photoassimilate export associated with massive callose deposition in transfer cells of the phloem. To further understand the roles of tocopherols in LT induced TCW development we compared the global transcript profiles of vte2 and wild-type leaves during LT treatment. Tocopherol deficiency had no significant impact on global gene expression in permissive conditions, but significantly affected expression of 77 genes after 48 h of LT treatment. In vte2 relative to wild type, genes associated with solute transport were repressed, while those involved in various pathogen responses and cell wall modifications, including two members of callose synthase gene family, GLUCAN SYNTHASE LIKE 4 (GSL4) and GSL11, were induced. However, introduction of gsl4 or gsl11 mutations individually into the vte2 background did not suppress callose deposition or the overall LT-induced phenotypes of vte2. Intriguingly, introduction of a mutation disrupting GSL5, the major GSL responsible for pathogen-induced callose deposition, into vte2 substantially reduced vascular callose deposition at LT, but again had no effect on the photoassimilate export phenotype of LT-treated vte2. These results suggest that GSL5 plays a major role in TCW callose deposition in LT-treated vte2 but that this GSL5-dependent callose deposition is not the primary cause of the impaired photoassimilate export phenotype.

No MeSH data available.


Related in: MedlinePlus

A gene tree of the 77 genes significantly altered in 48 h-LT-treated vte2 relative to Col (adjusted p-value < 0.05). The color bar represents expression levels (log2), with green to red being low to high expression. The groups (labeled as I, II, III, and IV) were based on general expression patterns across Col and vte2 at three time points of LT treatment. Genes showing opposite directions of expression from 0 to 48 h of LT treatment in Col and vte2 are highlighted in red (induced in vte2) or blue (repressed in vte2). See text for additional details.
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Figure 2: A gene tree of the 77 genes significantly altered in 48 h-LT-treated vte2 relative to Col (adjusted p-value < 0.05). The color bar represents expression levels (log2), with green to red being low to high expression. The groups (labeled as I, II, III, and IV) were based on general expression patterns across Col and vte2 at three time points of LT treatment. Genes showing opposite directions of expression from 0 to 48 h of LT treatment in Col and vte2 are highlighted in red (induced in vte2) or blue (repressed in vte2). See text for additional details.

Mentions: After 48 h at LT, 77 probe sets were found to be significantly different between vte2 and Col: 49 genes were significantly induced (Table 1) and 28 were significantly repressed (Table 2) in vte2 relative to Col. The expression patterns of these 77 genes across all time points are visualized in the gene tree in Figure 2. As discussed above, before LT treatment (0 h) expression levels of all genes are very similar between Col and vte2 and changed differently between genotypes after LT treatment. Group I contains 43 genes whose expression is generally low at 0 h and induced in both Col and vte2 after LT treatment, with induction in vte2 being stronger and more persistent. Group II contains 17 genes whose expression is somewhat high at 0 h and then more strongly induced or repressed in vte2 after LT treatment compared to Col. Group III (12 genes) and IV (5 genes) are expressed at moderately and very high levels at 0 h, respectively, and both repressed at LT more strongly and persistently in vte2 than Col. Several genes in groups I, II, and III show opposite expression patterns in vte2 and Col from 0 to 48 h of LT treatment (highlighted in red for induced or blue for repressed in vte2 relative to Col, respectively) and are particularly interesting as they represent potential “marker genes” that are specifically impacted by tocopherol deficiency at LT.


Role of callose synthases in transfer cell wall development in tocopherol deficient Arabidopsis mutants.

Maeda H, Song W, Sage T, Dellapenna D - Front Plant Sci (2014)

A gene tree of the 77 genes significantly altered in 48 h-LT-treated vte2 relative to Col (adjusted p-value < 0.05). The color bar represents expression levels (log2), with green to red being low to high expression. The groups (labeled as I, II, III, and IV) were based on general expression patterns across Col and vte2 at three time points of LT treatment. Genes showing opposite directions of expression from 0 to 48 h of LT treatment in Col and vte2 are highlighted in red (induced in vte2) or blue (repressed in vte2). See text for additional details.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3928550&req=5

Figure 2: A gene tree of the 77 genes significantly altered in 48 h-LT-treated vte2 relative to Col (adjusted p-value < 0.05). The color bar represents expression levels (log2), with green to red being low to high expression. The groups (labeled as I, II, III, and IV) were based on general expression patterns across Col and vte2 at three time points of LT treatment. Genes showing opposite directions of expression from 0 to 48 h of LT treatment in Col and vte2 are highlighted in red (induced in vte2) or blue (repressed in vte2). See text for additional details.
Mentions: After 48 h at LT, 77 probe sets were found to be significantly different between vte2 and Col: 49 genes were significantly induced (Table 1) and 28 were significantly repressed (Table 2) in vte2 relative to Col. The expression patterns of these 77 genes across all time points are visualized in the gene tree in Figure 2. As discussed above, before LT treatment (0 h) expression levels of all genes are very similar between Col and vte2 and changed differently between genotypes after LT treatment. Group I contains 43 genes whose expression is generally low at 0 h and induced in both Col and vte2 after LT treatment, with induction in vte2 being stronger and more persistent. Group II contains 17 genes whose expression is somewhat high at 0 h and then more strongly induced or repressed in vte2 after LT treatment compared to Col. Group III (12 genes) and IV (5 genes) are expressed at moderately and very high levels at 0 h, respectively, and both repressed at LT more strongly and persistently in vte2 than Col. Several genes in groups I, II, and III show opposite expression patterns in vte2 and Col from 0 to 48 h of LT treatment (highlighted in red for induced or blue for repressed in vte2 relative to Col, respectively) and are particularly interesting as they represent potential “marker genes” that are specifically impacted by tocopherol deficiency at LT.

Bottom Line: However, introduction of gsl4 or gsl11 mutations individually into the vte2 background did not suppress callose deposition or the overall LT-induced phenotypes of vte2.Intriguingly, introduction of a mutation disrupting GSL5, the major GSL responsible for pathogen-induced callose deposition, into vte2 substantially reduced vascular callose deposition at LT, but again had no effect on the photoassimilate export phenotype of LT-treated vte2.These results suggest that GSL5 plays a major role in TCW callose deposition in LT-treated vte2 but that this GSL5-dependent callose deposition is not the primary cause of the impaired photoassimilate export phenotype.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Michigan State University East Lansing, MI, USA ; Cell and Molecular Biology Program, Michigan State University East Lansing, MI, USA ; Department of Botany, University of Wisconsin-Madison Madison, WI, USA.

ABSTRACT
Tocopherols (vitamin E) are lipid-soluble antioxidants produced by all plants and algae, and many cyanobacteria, yet their functions in these photosynthetic organisms are still not fully understood. We have previously reported that the vitamin E deficient 2 (vte2) mutant of Arabidopsis thaliana is sensitive to low temperature (LT) due to impaired transfer cell wall (TCW) development and photoassimilate export associated with massive callose deposition in transfer cells of the phloem. To further understand the roles of tocopherols in LT induced TCW development we compared the global transcript profiles of vte2 and wild-type leaves during LT treatment. Tocopherol deficiency had no significant impact on global gene expression in permissive conditions, but significantly affected expression of 77 genes after 48 h of LT treatment. In vte2 relative to wild type, genes associated with solute transport were repressed, while those involved in various pathogen responses and cell wall modifications, including two members of callose synthase gene family, GLUCAN SYNTHASE LIKE 4 (GSL4) and GSL11, were induced. However, introduction of gsl4 or gsl11 mutations individually into the vte2 background did not suppress callose deposition or the overall LT-induced phenotypes of vte2. Intriguingly, introduction of a mutation disrupting GSL5, the major GSL responsible for pathogen-induced callose deposition, into vte2 substantially reduced vascular callose deposition at LT, but again had no effect on the photoassimilate export phenotype of LT-treated vte2. These results suggest that GSL5 plays a major role in TCW callose deposition in LT-treated vte2 but that this GSL5-dependent callose deposition is not the primary cause of the impaired photoassimilate export phenotype.

No MeSH data available.


Related in: MedlinePlus