Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetically engineered tobacco (Nicotiana tabacum L.) with the ability to synthesis glycinebetaine (GB) in chloroplasts was established by introducing the BADH gene for betaine aldehyde dehydrogenase from spinach (Spinacia oleracea L.). The genetic engineering resulted in enhanced tolerance of growth of young seedlings to salt stress. This increased tolerance was not due to improved water status, since there were no significant differences in accumulation of sodium and chloride, leaf water potential, and relative water content between wild type and transgenic plants under salt stress. Salt stress resulted in a decrease in CO2 assimilation and such a decrease was much greater in wild type plants than in transgenic plants. Though salt stress showed no damage to PSII, there were a decrease in the maximal PSII electron transport rate in vivo and an increase in non-photochemical quenching (NPQ) and these changes were greater in wild type plants than in transgenic plants. In addition, salt stress inhibited the activities of ribulose 1,5-bisphosphate carboxylase/oxygenase, chloroplastic fructose-1,6-bisphosphatase, fructose-1,6-bisphosphate aldolase, and phosphoribulokinase and such a decrease was also greater in wild type plants than in transgenic plants, suggesting that GB protects these enzymes against salt stress. However, there were no significant changes in the activities of phosphoglycerate kinase, triose phosphate isomerase, ribulose-5-phosphate isomerase, transketolase, and sedoheptulose-1,7-bisphosphatase in both wild type and transgenic plants. The results in this study suggest that enhanced tolerance of CO2 assimilation to salt stress may be one of physiological bases for increased tolerance of growth of transgenic plants to salt stress.
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PMID:Genetic engineering of the biosynthesis of glycinebetaine leads to increased tolerance of photosynthesis to salt stress in transgenic tobacco plants. 1797 34

Burkholderia pseudomallei primary diagnostic cultures demonstrate colony morphology variation associated with expression of virulence and adaptation proteins. This study aims to examine the ability of B. pseudomallei colony variants (wild type [WT] and small colony variant [SCV]) to survive and replicate intracellularly in A549 cells and to identify the alterations in the protein expression of these variants, post-exposure to the A549 cells. Intracellular survival and cytotoxicity assays were performed followed by proteomics analysis using two-dimensional gel electrophoresis. B. pseudomallei SCV survive longer than the WT. During post-exposure, among 259 and 260 protein spots of SCV and WT, respectively, 19 were differentially expressed. Among SCV post-exposure up-regulated proteins, glyceraldehyde 3-phosphate dehydrogenase, fructose-bisphosphate aldolase (CbbA) and betaine aldehyde dehydrogenase were associated with adhesion and virulence. Among the down-regulated proteins, enolase (Eno) is implicated in adhesion and virulence. Additionally, post-exposure expression profiles of both variants were compared with pre-exposure. In WT pre- vs post-exposure, 36 proteins were differentially expressed. Of the up-regulated proteins, translocator protein, Eno, nucleoside diphosphate kinase (Ndk), ferritin Dps-family DNA binding protein and peptidyl-prolyl cis-trans isomerase B were implicated in invasion and virulence. In SCV pre- vs post-exposure, 27 proteins were differentially expressed. Among the up-regulated proteins, flagellin, Eno, CbbA, Ndk and phenylacetate-coenzyme A ligase have similarly been implicated in adhesion, invasion. Protein profiles differences post-exposure provide insights into association between morphotypic and phenotypic characteristics of colony variants, strengthening the role of B. pseudomallei morphotypes in pathogenesis of melioidosis.
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PMID:Altered Proteome of Burkholderia pseudomallei Colony Variants Induced by Exposure to Human Lung Epithelial Cells. 2599 27