EC Number   |
General Information |
Reference |
|---|
    2.7.7.41 | evolution |
both CDP-diacylglycerol synthases Tam41 and Cds1 are highly conserved proteins, yet their origins seem to be different. The N-terminal portion of Tam41 possesses the NTase (Nucleotide Transferase) fold, which is consistent with the CDP-DAG synthase function of Tam41. In contrast, Cds1 exhibits the CDP-DAG synthase i.e. NTase activity, yet it does not contain the NTase fold. Cds1 and Tam41 have developed their own commitment to lipid biosynthetic pathways operating in two evolutionary distinct organelles, the endoplasmic reticulum and mitochondria, during evolution of eukaryotic cells |
738000 |
| 2.7.7.41 | evolution |
Cds1 is an evolutionarily conserved protein |
-, 739033 |
| 2.7.7.41 | evolution |
isoforms of CDS are located in plastids, mitochondria and the endomembrane system of plants and are encoded by five genes in Arabidopsis. Two genes have previously been shown to code for the plastidial isoforms which are indispensable for the biosynthesis of plastidial phosphatidylglycerol, and thus biogenesis and function of thylakoid membranes. the extraplastidial CDS isoforms, encoded by CDS1 and CDS2 which are constitutively expressed contrary to CDS3. These closely related CDS genes code for membrane proteins located in the endoplasmic reticulum and possess very similar enzymatic properties |
739305 |
| 2.7.7.41 | evolution |
Trypanosoma cruzi and Leishmaniasp. have both a eukaryotic and prokaryotic version, but Trypanosoma brucei has likely lost its prokaryotic homologue in the recent past |
-, 741020 |
| 2.7.7.41 | malfunction |
biochemical phenotype of the TbCDS conditional knockout, overvie. Lipid extracts from TbCDS CKO have a similar distribution of molecular species to that of wild-type cells across the phospholipid classes to that of wild-type cells, but an increase in diacylglycerols and triacylglycerols i detected. The decrease in CDS activity causes a marked reduction in phosphatidylinositol levels, the disproportional reduction implies the C36:1 species turns over faster than the C40:4 species. Incorporation of [3H]inositol into phosphatidylinositol and phosphatidylinositol phosphate seems relatively unaffected in the TbCDS CKO, but the mutant shows a significant reduction in flux through the GPI pathway |
-, 741020 |
| 2.7.7.41 | malfunction |
cycling bbl1 mutant cells deficient in the function of the endoplasmic reticlum-resident CDP-DG synthase Cds1 exhibit markedly increased triacylglycerol content and assemble large lipid droplets closely associated with the endoplasmic reticlum membranes. These unusual structures recruit the triacylglycerol synthesis machinery and grow by expansion rather than by fusion. Interfering with the CDP-DG route of phosphatidic acid utilization rewires cellular metabolism to adopt a triacylglycerol-rich lifestyle reliant on the Kennedy pathway. The bbl1 mutant enzyme is catalytically deficient, penotype, overview |
-, 739033 |
| 2.7.7.41 | malfunction |
cycling cells deficient in the function of the endoplasmic reticlum-resident CDP-DG synthase Cds1 exhibit markedly increased triacylglycerol content and assemble large lipid droplets closely associated with the endoplasmic reticlum membranes. These unusual structures recruit the triacylglycerol synthesis machinery and grow by expansion rather than by fusion. Interfering with the CDP-DG route of phosphatidic acid utilization rewires cellular metabolism to adopt a triacylglycerol-rich lifestyle reliant on the Kennedy pathway |
-, 739033 |
| 2.7.7.41 | malfunction |
enzyme knockdown results in decreased mitochondrial CDP diacylglycerol synthase activity, decreased cardiolipin levels and a decrease in oxygen consumption |
760639 |
| 2.7.7.41 | malfunction |
enzyme knockout causes abnormal heart development, specifically a defect in heart valve formation |
761129 |
| 2.7.7.41 | malfunction |
enzyme mutants show a defective growth due to impaired replication |
761476 |
