The Experts below are selected from a list of 2037 Experts worldwide ranked by ideXlab platform
Yasuyuki Igarashi - One of the best experts on this subject based on the ideXlab platform.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
The Biochemical journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Deltalcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
Biochemical Journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Δlcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
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Lipid asymmetry of the eukaryotic plasma membrane : Functions and related enzymes
Biological & pharmaceutical bulletin, 2006Co-Authors: Mika Ikeda, Akio Kihara, Yasuyuki IgarashiAbstract:Biological membranes are composed of Lipid bilayers. Major Lipid components of the eukaryotic plasma membrane include glycerophosphoLipids, sphingoLipids, and cholesterol. Lipids are irregularly distributed between the two leaflets, thus causing Lipid asymmetry, or within the same leaflet, forming a Lipid Microdomain. GlycerophosphoLipids and sphingoLipids both contribute to the Lipid asymmetry, whereas cholesterol and sphingoLipids form Lipid Microdomains. Maintenance of proper Lipid asymmetry is required for the mechanical stability of the membrane and for vesicular transport. On the other hand, local or global changes in Lipid asymmetry are important for cell cycle progression, apoptosis, and platelet coagulation. Three classes of Lipid translocases, P-type ATPases, ABC transporters, and scramblases, are known to be involved in the regulation of Lipid asymmetry. In this review, we describe the physiological and pathological functions of Lipid asymmetry and the current knowledge of Lipid translocases.
E. J. Kremer - One of the best experts on this subject based on the ideXlab platform.
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disruption of the coxsackievirus and adenovirus receptor homodimeric interaction triggers Lipid Microdomain and dynamin dependent endocytosis and lysosomal targeting
Journal of Biological Chemistry, 2014Co-Authors: S. Salinas, C. Zussy, F. Loustalot, D. Henaff, G. Menendez, P. E. Morton, M. Parsons, G. Schiavo, E. J. KremerAbstract:The coxsackievirus and adenovirus receptor (CAR) serves as a docking factor for some adenovirus (AdV) types and group B coxsackieviruses. Its role in AdV internalization is unclear as studies suggest that its intracellular domain is dispensable for some AdV infection. We previously showed that in motor neurons, AdV induced CAR internalization and co-transport in axons, suggesting that CAR was linked to endocytic and long-range transport machineries. Here, we characterized the mechanisms of CAR endocytosis in neurons and neuronal cells. We found that CAR internalization was Lipid Microdomain-, actin-, and dynamin-dependent, and subsequently followed by CAR degradation in lysosomes. Moreover, ligands that disrupted the homodimeric CAR interactions in its D1 domains triggered an internalization cascade involving sequences in its intracellular tail.
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Disruption of the coxsackievirus and adenovirus receptor- homodimeric interaction triggers Lipid Microdomain- and dynamin-dependent endocytosis and lysosomal targeting
Journal of Biological Chemistry, 2013Co-Authors: S. Salinas, C. Zussy, F. Loustalot, D. Henaff, G. Menendez, P. E. Morton, M. Parsons, G. Schiavo, E. J. KremerAbstract:The coxsackievirus and adenovirus receptor (CAR) serves as a docking factor for some adenovirus (AdV) types and group B coxsackieviruses. Its role in AdV internalisation is unclear as studies suggest that its intracellular domain is dispensable for some AdV serotype infection. We previously showed that in motor neurons, an adenovirus induced CAR internalisation, and their co-transport in axons, suggesting that CAR was linked to endocytic and long-range transport machineries. Here, we characterised the mechanisms of CAR endocytosis in neurons and neuronal cells. We show that ligands that disrupted the homodimeric CAR interactions in its D1 domains triggered an internalisation cascade involving sequences in its intracellular tail. CAR-associated internalisation was also Lipid Microdomain, actin- and dynamin-dependent, and subsequently followed by CAR degradation by lysosomes.
Akio Kihara - One of the best experts on this subject based on the ideXlab platform.
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biosynthesis of the anti Lipid Microdomain sphingoid base 4 14 sphingadiene by the ceramide desaturase fads3
The FASEB Journal, 2020Co-Authors: Keisuke Jojima, Mai Edagawa, Megumi Sawai, Yusuke Ohno, Akio KiharaAbstract:SphingoLipids are multifunctional Lipids. Among the sphingoLipid-component sphingoid bases, 4,14-sphingadiene (SPD) is unique such that it has a cis double bond with a bent structure. Although SPD was discovered half a century ago, its tissue distribution, biosynthesis, and degradation remain poorly understood. Here, we established a specific and quantitative method for SPD measurement and found that SPD exists in a wide range of mammalian tissues. SPD was especially abundant in kidney, where the amount of SPD was ~2/3 of sphingosine, the most abundant sphingoid base in mammals. Although SPD is metabolized to ceramides and SPD 1-phosphate with almost the same efficiency as sphingosine, it is less susceptible to degradation by a cleavage reaction, at least in vitro. We identified the fatty acid desaturase family protein FADS3 as a ceramide desaturase that produces SPD ceramides by desaturating ceramides containing sphingosine. SPD sphingoLipids were preferentially localized outside Lipid Microdomains, suggesting that SPD has different functions compared to other sphingoid bases in the formation of Lipid Microdomains. In summary, we revealed the biosynthesis and degradation pathways of SPD and its characteristic membrane localization. Our findings contribute to the elucidation of the molecular mechanism underlying the generation of sphingoLipid diversity.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
The Biochemical journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Deltalcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
Biochemical Journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Δlcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
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Lipid asymmetry of the eukaryotic plasma membrane : Functions and related enzymes
Biological & pharmaceutical bulletin, 2006Co-Authors: Mika Ikeda, Akio Kihara, Yasuyuki IgarashiAbstract:Biological membranes are composed of Lipid bilayers. Major Lipid components of the eukaryotic plasma membrane include glycerophosphoLipids, sphingoLipids, and cholesterol. Lipids are irregularly distributed between the two leaflets, thus causing Lipid asymmetry, or within the same leaflet, forming a Lipid Microdomain. GlycerophosphoLipids and sphingoLipids both contribute to the Lipid asymmetry, whereas cholesterol and sphingoLipids form Lipid Microdomains. Maintenance of proper Lipid asymmetry is required for the mechanical stability of the membrane and for vesicular transport. On the other hand, local or global changes in Lipid asymmetry are important for cell cycle progression, apoptosis, and platelet coagulation. Three classes of Lipid translocases, P-type ATPases, ABC transporters, and scramblases, are known to be involved in the regulation of Lipid asymmetry. In this review, we describe the physiological and pathological functions of Lipid asymmetry and the current knowledge of Lipid translocases.
Motohiro Tani - One of the best experts on this subject based on the ideXlab platform.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
The Biochemical journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Deltalcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
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Rescue of cell growth by sphingosine with disruption of Lipid Microdomain formation in Saccharomyces cerevisiae deficient in sphingoLipid biosynthesis.
Biochemical Journal, 2006Co-Authors: Motohiro Tani, Akio Kihara, Yasuyuki IgarashiAbstract:In the yeast Saccharomyces cerevisiae, sphingoLipids are essential for cell growth. Inactivation of sphingoLipid biosynthesis, such as by disrupting the serine palmitoyltransferase gene (LCB2), is lethal, but cells can be rescued by supplying an exogenous LCB (long-chain base) like PHS (phytosphingosine) or DHS (dihydrosphingosine). In the present study, supplying SPH (sphingosine), an unnatural LCB for yeast, similarly rescued the Δlcb2 cells, but only when SPH 1-phosphate production was inhibited by deleting the LCB kinase gene LCB4. Exogenously added SPH was adequately converted into phosphoinositol-containing complex sphingoLipids. Interestingly, cells carrying SPH-based sphingoLipids exhibited a defect in the association of Pma1p with Triton X-100-insoluble membrane fractions, and displayed sensitivities to both Ca2+ and hygromycin B. These results suggest that the SPH-based sphingoLipids in these cells have properties that differ from those of the PHS- or DHS-based sphingoLipids in regard to Lipid Microdomain formation, leading to abnormal sensitivities towards certain environmental stresses. The present paper is the first report showing that in sphingoLipid-deficient S. cerevisiae, the requirement for LCB can be fulfilled by exogenous SPH, although this supplement results in failure of Lipid Microdomain formation.
Jozef Samaj - One of the best experts on this subject based on the ideXlab platform.
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Lipid Microdomain polarization is required for nadph oxidase dependent ros signaling in picea meyeri pollen tube tip growth
Plant Journal, 2009Co-Authors: Ruili Li, Liang Zhang, Qinli Wang, Karsten Niehaus, Frantisek Baluska, Jozef SamajAbstract:*† SUMMARY The polarization of sterol-enriched Lipid Microdomains has been linked to morphogenesis and cell movement in diverse cell types. Recent biochemical evidence has confirmed the presence of Lipid Microdomains in plant cells; however, direct evidence for a functional link between these Microdomains and plant cell growth is still lacking. Here, we reported the involvement of Lipid Microdomains in NADPH oxidase (NOX)-dependent reactive oxygen species (ROS) signaling in Picea meyeri pollen tube growth. Staining with di-4-ANEPPDHQ or filipin revealed that sterol-enriched Microdomains were polarized to the growing tip of the pollen tube. Sterol sequestration with filipin disrupted membrane Microdomain polarization, depressed tip-based ROS formation, dissipated tip-focused cytosolic Ca 2+ gradient and thereby arrested tip growth. NOX clustered at the growing tip, and corresponded with the ordered membrane domains. Immunoblot analysis and native gel assays demonstrated that NOX was partially associated with detergent-resistant membranes and, furthermore, that NOX in a sterol-dependent fashion depends on membrane Microdomains for its enzymatic activity. In addition, in vivo time-lapse imaging revealed the coexistence of a steep tip-high apical ROS gradient and subapical ROS production, highlighting the reported signaling role for ROS in polar cell growth. Our results suggest that the polarization of Lipid Microdomains to the apical plasma membrane, and the inclusion of NOX into these domains, contribute, at least in part, to the ability to grow in a highly polarized manner to form pollen tubes.
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Lipid Microdomain polarization is required for NADPH oxidase-dependent ROS signaling in Picea meyeri pollen tube tip growth
The Plant journal : for cell and molecular biology, 2009Co-Authors: Peng Liu, Liang Zhang, Qinli Wang, Karsten Niehaus, Frantisek Baluska, Jozef Samaj, Jinxing LinAbstract:*† SUMMARY The polarization of sterol-enriched Lipid Microdomains has been linked to morphogenesis and cell movement in diverse cell types. Recent biochemical evidence has confirmed the presence of Lipid Microdomains in plant cells; however, direct evidence for a functional link between these Microdomains and plant cell growth is still lacking. Here, we reported the involvement of Lipid Microdomains in NADPH oxidase (NOX)-dependent reactive oxygen species (ROS) signaling in Picea meyeri pollen tube growth. Staining with di-4-ANEPPDHQ or filipin revealed that sterol-enriched Microdomains were polarized to the growing tip of the pollen tube. Sterol sequestration with filipin disrupted membrane Microdomain polarization, depressed tip-based ROS formation, dissipated tip-focused cytosolic Ca 2+ gradient and thereby arrested tip growth. NOX clustered at the growing tip, and corresponded with the ordered membrane domains. Immunoblot analysis and native gel assays demonstrated that NOX was partially associated with detergent-resistant membranes and, furthermore, that NOX in a sterol-dependent fashion depends on membrane Microdomains for its enzymatic activity. In addition, in vivo time-lapse imaging revealed the coexistence of a steep tip-high apical ROS gradient and subapical ROS production, highlighting the reported signaling role for ROS in polar cell growth. Our results suggest that the polarization of Lipid Microdomains to the apical plasma membrane, and the inclusion of NOX into these domains, contribute, at least in part, to the ability to grow in a highly polarized manner to form pollen tubes.