EC Number   |
General Information |
Reference |
|---|
    4.1.1.65 | malfunction |
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 |
-, 703770 |
| 4.1.1.65 | malfunction |
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 |
-, 702464 |
| 4.1.1.65 | malfunction |
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 |
705619 |
| 4.1.1.65 | malfunction |
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. |
-, 703515 |
| 4.1.1.65 | malfunction |
psd1 and psd2 deletion mutants exhibit defects in filamentous growth |
705791 |
| 4.1.1.65 | malfunction |
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 |
727932 |
| 4.1.1.65 | metabolism |
the stability of endogenous Psd1 is influenced by inner membrane protease Yme1 |
748652 |
| 4.1.1.65 | 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 |
-, 748671 |
| 4.1.1.65 | physiological function |
enzyme is able to complement a Saccharomyces cerevisiae PSD mutant lacking PSD1 and PSD2 and DPL1 activities |
748688 |
| 4.1.1.65 | physiological function |
enzyme is responsible for remodeling of human phosphatidylserine to bacterial phosphatidylethanolamine in human pathogen Chlamydia trachomatis |
-, 746468 |
