4.1.1.65: phosphatidylserine decarboxylase
This is an abbreviated version!
For detailed information about phosphatidylserine decarboxylase, go to the full flat file.
Word Map on EC 4.1.1.65
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4.1.1.65
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phospholipid
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phosphatidylcholine
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kennedy
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cdp-ethanolamine
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decarboxylases
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3hserine
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ptdetn
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cdp-diacylglycerol
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phosphatidylglycerophosphate
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dowhan
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spinothalamic
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base-exchange
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aminophospholipids
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interorganelle
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cdp-diglyceride
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medicine
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analysis
- 4.1.1.65
- phospholipid
- phosphatidylcholine
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kennedy
- cdp-ethanolamine
- decarboxylases
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3hserine
-
ptdetn
- cdp-diacylglycerol
- phosphatidylglycerophosphate
-
dowhan
-
spinothalamic
-
base-exchange
-
aminophospholipids
-
interorganelle
- cdp-diglyceride
- medicine
- analysis
Reaction
Synonyms
CT699, Decarboxylase, phosphatidylserine, phosphatidyl serine decarboxylase, Phosphatidylserine decarboxylase, phosphatidylserine decarboxylase 1, phosphatidylserine decarboxylase 2, phosphatidylserine decarboxylase2, PISD, PKH_072580, PS decarboxylase, PSD, PSD1, Psd1 enzyme, Psd1p, PSD2, Psd2p, PSD3, PSDC, Tb927.9.10080, type I PtdSer decarboxylase
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General Information on EC 4.1.1.65 - phosphatidylserine decarboxylase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
metabolism
the stability of endogenous Psd1 is influenced by inner membrane protease Yme1
physiological function
malfunction
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deletion of isoform PSD1 causes loss of PSD activity in mitochondria, a severe growth defect on minimal media, and depletion of cellular and mitochondrial phosphatidylethanolamine levels. This defect cannot be compensated by Psd2p. In the homogenate of psd2DELTA, the PSD activity is only slightly reduced, whereas in psd1DELTA total PSD activity is only 25% of wild type
malfunction
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deletion of PSD1 and/or PSD2 leads to depletion of total cellular and plasma membrane phosphatidylethanolamine level, whereas mutation in the other pathways has practically no effect
malfunction
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loss of Psd2 causes cells to acquire sensitivity to cadmium even though Psd1 remains intact, loss of Psd2 causes a specific reduction in vacuolar membrane phosphatidylethanolamine levels, whereas total phosphatidylethanolamine levels are not significantly affected
malfunction
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mutants carrying deletions in any one or two psd genes are viable in complex rich medium and synthetic defined minimal medium. However, mutants carrying deletions in all three psd genes (psd1-3DELTA mutants) grow slowly in rich medium and are inviable in minimal medium. psd1-3_DELTAcells appear morphologically indistinguishable from wild type cells in medium supplemented with ethanolamine, but when cultured in nonsupplemented medium, they produce high frequencies of abnormally shaped cells as well as cells exhibiting severe septation defects, including multiple, mispositioned, deformed, and misoriented septa.
malfunction
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psd1 and psd2 deletion mutants exhibit defects in filamentous growth
malfunction
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the psd1-deficient strain shows reduced fusion kinetics and also has impaired mitochondrial activity such as oxidative phosphorylation and reduced mitochondrial ATP levels. The loss of Psd1 also impairs the biogenesis of s-Mgm1, a protein essential for mitochondrial fusion
malfunction
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deletion of PSD1 and/or PSD2 leads to depletion of total cellular and plasma membrane phosphatidylethanolamine level, whereas mutation in the other pathways has practically no effect
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malfunction
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deletion of isoform PSD1 causes loss of PSD activity in mitochondria, a severe growth defect on minimal media, and depletion of cellular and mitochondrial phosphatidylethanolamine levels. This defect cannot be compensated by Psd2p. In the homogenate of psd2DELTA, the PSD activity is only slightly reduced, whereas in psd1DELTA total PSD activity is only 25% of wild type
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malfunction
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mutants carrying deletions in any one or two psd genes are viable in complex rich medium and synthetic defined minimal medium. However, mutants carrying deletions in all three psd genes (psd1-3DELTA mutants) grow slowly in rich medium and are inviable in minimal medium. psd1-3_DELTAcells appear morphologically indistinguishable from wild type cells in medium supplemented with ethanolamine, but when cultured in nonsupplemented medium, they produce high frequencies of abnormally shaped cells as well as cells exhibiting severe septation defects, including multiple, mispositioned, deformed, and misoriented septa.
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physiological function
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phosphatidylserine decarboxylase is a Toll-like receptor 4 agonist, phosphatidylserine decarboxylase in concentrations as low as 100 ng/ml stimulates RAW264.7 murine macrophage cells and primary peritoneal macrophage cells to secrete tissue necrosis factor alpha and interleukin-6, respectively. PSD induces the production of interleukin-6, in part, via its enzymatic activity
physiological function
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phosphatidylserine decarboxylase is essential for cell wall integrity and virulence in Candida albicans
physiological function
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the mitochondrial Psd1 provides roughly 70% of the phosphatidylethanolamine biosynthesis in the cell with Psd2 carrying out the remainder, Psd2 action enhances Ycf1-dependent transport activity
physiological function
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the psd1, psd2, and psd3 gene products share overlapping functions essential for the normal growth of Schizosaccharomyces pombe cells
physiological function
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isoform PSD1 reduces externalized phosphatidylserine on host cells, enabling evasion of phagocytosis
physiological function
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phosphatidylethanolamine from phosphatidylserine decarboxylase2 (PSD2) is essential for autophagy under cadmium stress in Saccharomyces cerevisiae. Overexpression of PSD2 confers resistance to cadmium
physiological function
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Psd1 is required for normal mitochondrial morphology, proper mitochondrial fusion during yeast mating, and proper mitochondrial activity
physiological function
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the enzyme is required for an optimal parasite growth and replication
physiological function
after 4 days of gene silencing, procyclic forms of Trypanosoma brucei show a growth defect compared to control parasites, while growth of PSD-depleted bloodstream forms is only slightly affected. In both life cycle forms, down-regulation of TbPSD leads to mitochondrial fragmentation and a decrease in ATP production via oxidative phosphorylation of more than 75% in PSD-depleted mitochondria
physiological function
enzyme is able to complement a Saccharomyces cerevisiae PSD mutant lacking PSD1 and PSD2 and DPL1 activities
physiological function
enzyme is responsible for remodeling of human phosphatidylserine to bacterial phosphatidylethanolamine in human pathogen Chlamydia trachomatis
physiological function
the plasma membrane of a isoforms Psd1/Psd2 double mutant strain displays increased membrane fluidity and reduced plasma membrane dipole potential. In comparison to wild-type, the apparent phase transition temperature is reduced by about 3°C in the mutant strain. The mutant shows high diffusion of fluorescent dye rhodamine 6G and radiolabelled fluconazole, resulting in an increased drug accumulation in the mutant cells, and in an increased susceptibility to azoles
physiological function
the plasma membrane of isoforms Psd1/Psd2 double mutant strain displays increased membrane fluidity and reduced plasma membrane dipole potential. In comparison to wild-type, the apparent phase transition temperature is reduced by about 3°C in the mutant strain. The mutant shows high diffusion of fluorescent dye rhodamine 6G and radiolabelled fluconazole, resulting in an increased drug accumulation in the mutant cells, and in an increased susceptibility to azoles
physiological function
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phosphatidylethanolamine from phosphatidylserine decarboxylase2 (PSD2) is essential for autophagy under cadmium stress in Saccharomyces cerevisiae. Overexpression of PSD2 confers resistance to cadmium
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physiological function
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enzyme is responsible for remodeling of human phosphatidylserine to bacterial phosphatidylethanolamine in human pathogen Chlamydia trachomatis
-
physiological function
-
the plasma membrane of a isoforms Psd1/Psd2 double mutant strain displays increased membrane fluidity and reduced plasma membrane dipole potential. In comparison to wild-type, the apparent phase transition temperature is reduced by about 3°C in the mutant strain. The mutant shows high diffusion of fluorescent dye rhodamine 6G and radiolabelled fluconazole, resulting in an increased drug accumulation in the mutant cells, and in an increased susceptibility to azoles
-
physiological function
-
the plasma membrane of isoforms Psd1/Psd2 double mutant strain displays increased membrane fluidity and reduced plasma membrane dipole potential. In comparison to wild-type, the apparent phase transition temperature is reduced by about 3°C in the mutant strain. The mutant shows high diffusion of fluorescent dye rhodamine 6G and radiolabelled fluconazole, resulting in an increased drug accumulation in the mutant cells, and in an increased susceptibility to azoles
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physiological function
Trypanosoma brucei 927/4 GUTat10.1
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after 4 days of gene silencing, procyclic forms of Trypanosoma brucei show a growth defect compared to control parasites, while growth of PSD-depleted bloodstream forms is only slightly affected. In both life cycle forms, down-regulation of TbPSD leads to mitochondrial fragmentation and a decrease in ATP production via oxidative phosphorylation of more than 75% in PSD-depleted mitochondria
-
physiological function
-
the psd1, psd2, and psd3 gene products share overlapping functions essential for the normal growth of Schizosaccharomyces pombe cells
-
physiological function
-
isoform PSD1 reduces externalized phosphatidylserine on host cells, enabling evasion of phagocytosis
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