Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
Substrates: LPLAT 7 prefers 20:4-CoA and 20:5-CoA as donors. Analysis of in vivo incorporation of exogenous fatty acids into Caenorhabditis elegans Products: -
phospholipase A2 (PLA2) plays a role in membrane phospholipid remodeling by coupling with re-acylation processes mediated by lysophospholipid acyltransferases (LPLATs) to generate sn-1/sn-2 fatty acid asymmetry of phospholipids. Lysophospholipids are acylated by LPLAT to generate phospholipids phosphatidic acid (PA), phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylglycerol (PG), and cardiolipin (CL) by LPLATs. In the Kennedy pathway, glycerol-3-phosphate (G3P) is first acylated by glycerol-phosphate acyltransferase (GPAT) to form lyso-PA (LPA), which is subsequently converted to PA by LPA-acyltransferase (LPAAT)
incorporation of exogenous PUFA into PI of the living worms and LPIAT activity in the microsomes are greatly reduced in mboa-7 mutants. Furthermore, the membrane fractions of transgenic worms expressing recombinant MBOA-7 and its human homologue exhibit remarkably increased LPIAT activity. Gene mboa-7 mutants have significantly lower eicosapentaenoic acid (EPA) levels in phosphatidylinositol (PI), and they exhibit larval arrest and egg-laying defects. Fatty acid composition of wild-type and mboa-7 mutants, overview
LPIAT1 deficiency induces abnormal brain morphology, delays neural migration, and reduces neurite outgrowth in mice. The size of LPIAT1-KO mice is significantly smaller than that of their littermates. The frequency of mice carrying the knockout mutation is lower than that expected by Mendelian genetics. Rs641738, a polymorphism in the LPIAT1 (MBOAT7) locus is reported to associate with hepatic inflammation and increased risk of fibrosis, nonalcoholic fatty liver disease, and alcohol related cirrhosis. This variant decreases LPIAT1 expression in the liver and changes PI compositions in the plasma. Other mutations are also reported to lead to intellectual disability, suggesting the importance of AA-containing phosphatidylinositol in the disease development
incorporation of exogenous PUFA into PI of the living worms and LPIAT activity in the microsomes are greatly reduced in mboa-7 mutants. Furthermore, the membrane fractions of transgenic worms expressing recombinant MBOA-7 and its human homologue exhibit remarkably increased LPIAT activity. Gene mboa-7 mutants have significantly lower eicosapentaenoic acid (EPA) levels in phosphatidylinositol (PI), and they exhibit larval arrest and egg-laying defects. Fatty acid composition of wild-type and mboa-7 mutants, overview
the enzyme is required for selective incorporation of polyunsaturated fatty acids (PUFAs) into phosphatidylinositol. Phosphatidylinositol (PI) is a component of membrane phospholipids, and it functions both as a signaling molecule and as a compartment-specific localization signal in the form of polyphosphoinositides. Arachidonic acid (AA) is the predominant fatty acid in the sn-2 position of PI in mammals. LysoPI acyltransferase (LPIAT) is thought to catalyze formation of AA-containing PI
the enzyme is required for selective incorporation of polyunsaturated fatty acids (PUFAs) into phosphatidylinositol. Phosphatidylinositol (PI) is a component of membrane phospholipids, and it functions both as a signaling molecule and as a compartment-specific localization signal in the form of polyphosphoinositides. Arachidonic acid (AA) is the predominant fatty acid in the sn-2 position of PI in mammals. LysoPI acyltransferase (LPIAT) is thought to catalyze formation of AA-containing PI
the enzyme is required for selective incorporation of polyunsaturated fatty acids (PUFAs) into phosphatidylinositol. Phosphatidylinositol (PI) is a component of membrane phospholipids, and it functions both as a signaling molecule and as a compartment-specific localization signal in the form of polyphosphoinositides. Arachidonic acid (AA) is the predominant fatty acid in the sn-2 position of PI in mammals. LysoPI acyltransferase (LPIAT) is thought to catalyze formation of AA-containing PI. In Caenorhabditis elegans, eicosapentaenoic acid (EPA) instead of AA is the predominant fatty acid in PI
the enzyme is required for selective incorporation of polyunsaturated fatty acids (PUFAs) into phosphatidylinositol. Phosphatidylinositol (PI) is a component of membrane phospholipids, and it functions both as a signaling molecule and as a compartment-specific localization signal in the form of polyphosphoinositides. Arachidonic acid (AA) is the predominant fatty acid in the sn-2 position of PI in mammals. LysoPI acyltransferase (LPIAT) is thought to catalyze formation of AA-containing PI. In Caenorhabditis elegans, eicosapentaenoic acid (EPA) instead of AA is the predominant fatty acid in PI
construction of mboa-7 mutants, the following mutations are used: fat-1(wa9), fat-3(wa22), fat-4(wa14), eri-1(mg366), and mboa-7(gk399). mboa-7(gk399) mutation is backcrossed at five times, phenotype, detailed overview. fat-4 fat-1 mutants, which do not produce AA(20:4n-6) and n-3 PUFAs such as EPA(20:5n-3), are viable and fertile, but they exhibited slow growth at 15°C. Dietary supplementation with arachidonic acid (AA) or eicosapentaenoic acid (EPA) leads to incorporation of these PUFAs into the phospholipid fractions of fat-4 fat-1 mutants, and it rescues the growth defects of this strain. Fatty acid composition of wild-type and mboa-7 mutants, overview
construction of mboa-7 mutants, the following mutations are used: fat-1(wa9), fat-3(wa22), fat-4(wa14), eri-1(mg366), and mboa-7(gk399). mboa-7(gk399) mutation is backcrossed at five times, phenotype, detailed overview. fat-4 fat-1 mutants, which do not produce AA(20:4n-6) and n-3 PUFAs such as EPA(20:5n-3), are viable and fertile, but they exhibited slow growth at 15°C. Dietary supplementation with arachidonic acid (AA) or eicosapentaenoic acid (EPA) leads to incorporation of these PUFAs into the phospholipid fractions of fat-4 fat-1 mutants, and it rescues the growth defects of this strain. Fatty acid composition of wild-type and mboa-7 mutants, overview
construction of mboa-7 mutants, the following mutations are used: fat-1(wa9), fat-3(wa22), fat-4(wa14), eri-1(mg366), and mboa-7(gk399). mboa-7(gk399) mutation is backcrossed at five times, phenotype, detailed overview. fat-4 fat-1 mutants, which do not produce AA(20:4n-6) and n-3 PUFAs such as EPA(20:5n-3), are viable and fertile, but they exhibited slow growth at 15°C. Dietary supplementation with arachidonic acid (AA) or eicosapentaenoic acid (EPA) leads to incorporation of these PUFAs into the phospholipid fractions of fat-4 fat-1 mutants, and it rescues the growth defects of this strain. Fatty acid composition of wild-type and mboa-7 mutants, overview
in cells transfected with hmboa-7 siRNA duplex, h-mboa-7 mRNA levels are reduced to about 30% of the level in control siRNA-transfected cells at 72 h after the transfection. Incorporation of [14C]AA into cellular PI is specifically reduced from 13.1% of the total radioactivity in control cells to 6.7% in the siRNA-transfected cells. Incorporation of [14C]EPA into PI is also reduced similar to that of [14C]AA in siRNA-transfected cells
in cells transfected with hmboa-7 siRNA duplex, h-mboa-7 mRNA levels are reduced to about 30% of the level in control siRNA-transfected cells at 72 h after the transfection. Incorporation of [14C]AA into cellular PI is specifically reduced from 13.1% of the total radioactivity in control cells to 6.7% in the siRNA-transfected cells. Incorporation of [14C]EPA into PI is also reduced similar to that of [14C]AA in siRNA-transfected cells
gene MBOAT7, cloning from HeLa cells, DNA and amino acid sequence determination and analysis, sequence comparisons, quantitative real-time reverse transcription PCR enzyme expression analysis
Caenorhabditis elegans mboa-7, a member of the MBOAT family, is required for selective incorporation of polyunsaturated fatty acids into phosphatidylinositol
Mol. Biol. Cell
19
1174-1184
2008
Caenorhabditis elegans (Q19468), Caenorhabditis elegans, Caenorhabditis elegans Bristol N2 (Q19468), Homo sapiens (Q96N66), Homo sapiens, Mus musculus (Q8CHK3)