EC Number   |
General Information |
Reference |
|---|
    2.7.8.8 | malfunction |
a phosphatidylserine synthase deletion mutant lacks phosphatidylserine, has decreased phosphatidylethanolamine, exhibits defects in cell wall integrity, mitochondrial function, filamentous growth, and is avirulent in a mouse model of systemic candidiasis |
705791 |
| 2.7.8.8 | malfunction |
disruption of PSS1 causes severe dwarfism, smaller lateral organs and reduced size of inflorescence meristem. Both cell division and cell elongation are affected in the pss1-1 mutant. The defect in meristem maintenance is recovered and the expression of WUS and CLV3 are restored in the pss1-1 clv1-1 double mutant. Both shootstemless (STM) and brevipedicellus (BP) are upregulated, and auxin distribution is disrupted in rosette leaves of pss1-1 mutant, expression of BP, which is also a regulator of internode development, is lost in the pss1-1 inflorescence stem. Phenotypes, detailed overview |
738817 |
| 2.7.8.8 | malfunction |
mutation of OsPSS-1 leads to compromised delivery of CESA4 and secGFP towards the cell surface, resulting in weakened intercellular adhesion and disorganized cell arrangement in parenchyma. The Dwarf phenotype of shortened uppermost internode 1 (sui1) is caused by mutations in phosphatidylserine synthase. The phenotype of sui1-4 is caused largely by the reduction in cellulose contents in the whole plant and detrimental delivery of pectins in the uppermost internode. sui1-4 plants exhibit compromised secretion. The mutants show reduced length of both panicles and internodes, especially the uppermost internode, accompanied with reduced fertility, decreased grain size and slightly increased tiller number, defective pectin secretion, detailed overview. A large amount of OsCESA4 remained in the cytoplasm in the mutant, most likely due to failure in delivery to the plasma membrane |
739446 |
| 2.7.8.8 | physiological function |
expression of Cho1 in a Saccharomyces cerevisiae Cho1 deletion mutant rescues the mutant's growth defect in the absence of ethanolamine supplementation. An Saccharomyces cerevisiae Cho1 deletion mutant expressing Cryptococcus neoformans Cho1 has phosphatidylserine synthase activity. Expression of Cho1 in Cryptococcus neoformans is essential for mitochondrial function and cell viability. Its deficiency cannot be complemented by ethanolamine or choline supplementation |
761508 |
| 2.7.8.8 | physiological function |
expression of Escherichia coli phosphatidylserine synthase PssA in various membrane compartments with distinct membrane topologies in yeast cells lacking phosphatidylserine synthase Cho1. PssA is able to complement loss of Cho1 when targeted to the endoplasmic reticulum, peroxisome, or lipid droplet membranes. Synthesised phosphatidylserine can be converted to phosphatidylethanolamine by Psd1, the mitochondrial phosphatidylserine decarboxylase. PssA which has been integrated into the mitochondrial inner membrane from the matrix side can partially complement the loss of Cho1 |
761073 |
| 2.7.8.8 | physiological function |
knockdown of PSS in Salicornia europaea suspension cells results in reduced phosphatidylserine content, decreased cell survival rate, and increased plasma membrane depolarization and K+ efflux in presence of 400 or 800 mM NaCl. The upregulation of PSS leads to increased phosphatidylserine and phosphatidylethanolamine levels and enhanced salt tolerance in Arabidopsis, along with a lower accumulation of reactive oxygen species, less membrane injury, less plasma membrane depolarization and higher K+/Na+ ratio in the transgenic lines than in wild-type |
762133 |
| 2.7.8.8 | physiological function |
phosphatidylserine synthase 1 is required for inflorescence meristem and organ development in Arabidopsis thaliana. Phosphatidylserine, a quantitatively minor membrane phospholipid, is involved in many biological processes besides its role in membrane structure, e.g. it is required for microspore development. Expression of both genes WUSCHEL (WUS) and CLAVATA3 (CLV3) depend on PSS1. PSS1 plays essential roles in inflorescence meristem maintenance through the WUS-CLV pathway, and in leaf and internode development by differentially regulating the class I KNOX genes. PSS1 is involved in a lot of developmental processes and is vital for postembryonic development of Arabidopsis thaliana. PSS1 regulates auxin distribution during leaf development |
738817 |
| 2.7.8.8 | physiological function |
phosphatidylserine synthase genes regulate the development of intercalary meristem for internode elongation and also the cell expansion of the panicle stem rachis in rice |
723504 |
| 2.7.8.8 | physiological function |
phosphatidylserine synthase1 is required for microspore development in Arabidopsis thaliana |
723425 |
| 2.7.8.8 | physiological function |
PSS1 regulates post-Golgi vesicle secretion to intercellular spaces. Mutation of PSS1 leads to compromised delivery of CESA4 and sec-GFP towards the cell surface, resulting in weakened intercellular adhesion and disorganized cell arrangement in parenchyma. The phenotype sui1-4 of PSS1 mutants is caused largely by the reduction in cellulose contents in the whole plant and detrimental delivery of pectins in the uppermost internode. PSS1 and product phosphatidylserine localize to organelles associated with exocytosis |
762210 |
