Glycine cleavage system in neurogenic regions
The glycine cleavage system (GCS) is the essential enzyme complex for degrading glycine and supplying 5,10‐methylenetetrahydrofolate for DNA synthesis. Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of bra...
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| Veröffentlicht in: | The European journal of neuroscience 2004-05, Vol.19 (9), p.2365-2370 |
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| container_title | The European journal of neuroscience |
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| creator | Ichinohe, Akiko Kure, Shigeo Mikawa, Sumiko Ueki, Takatoshi Kojima, Kanako Fujiwara, Kazuko Iinuma, Kazuie Matsubara, Yoichi Sato, Kohji |
| description | The glycine cleavage system (GCS) is the essential enzyme complex for degrading glycine and supplying 5,10‐methylenetetrahydrofolate for DNA synthesis. Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of brain malformations. Although high levels of glycine have been considered to cause the above‐mentioned problems, the detailed pathogenesis of this disease is still unknown. Here we show that GCS is abundantly expressed in rat embryonic neural stem/progenitor cells in the neuroepithelium, and this expression is transmitted to the radial glia–astrocyte lineage, with prominence in postnatal neurogenic regions. These data indicate that GCS plays important roles in neurogenesis, and suggest that disturbance of neurogenesis induced by deficiency of GCS may be the main pathogenesis of nonketotic hyperglycinemia. |
| doi_str_mv | 10.1111/j.0953-816X.2004.03345.x |
| format | Article |
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Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of brain malformations. Although high levels of glycine have been considered to cause the above‐mentioned problems, the detailed pathogenesis of this disease is still unknown. Here we show that GCS is abundantly expressed in rat embryonic neural stem/progenitor cells in the neuroepithelium, and this expression is transmitted to the radial glia–astrocyte lineage, with prominence in postnatal neurogenic regions. 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Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of brain malformations. Although high levels of glycine have been considered to cause the above‐mentioned problems, the detailed pathogenesis of this disease is still unknown. Here we show that GCS is abundantly expressed in rat embryonic neural stem/progenitor cells in the neuroepithelium, and this expression is transmitted to the radial glia–astrocyte lineage, with prominence in postnatal neurogenic regions. These data indicate that GCS plays important roles in neurogenesis, and suggest that disturbance of neurogenesis induced by deficiency of GCS may be the main pathogenesis of nonketotic hyperglycinemia.</description><subject>Amino Acid Oxidoreductases - genetics</subject><subject>Amino Acid Oxidoreductases - metabolism</subject><subject>Amino Acid Transport System X-AG - genetics</subject><subject>Amino Acid Transport System X-AG - metabolism</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Brain - cytology</subject><subject>Brain - physiology</subject><subject>Brain Chemistry</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cells, Cultured</subject><subject>Embryo, Mammalian</subject><subject>Epithelial Cells - cytology</subject><subject>Gene Expression Regulation, Developmental - physiology</subject><subject>glycine</subject><subject>glycine cleavage system</subject><subject>Immunohistochemistry - methods</subject><subject>Liver - enzymology</subject><subject>Multienzyme Complexes - genetics</subject><subject>Multienzyme Complexes - metabolism</subject><subject>neural stem cell</subject><subject>Neuroglia - enzymology</subject><subject>Neurons - enzymology</subject><subject>nonketotic hyperglycinemia</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Transferases - genetics</subject><subject>Transferases - metabolism</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEFPwjAUgBujEUT_gtnJ22a7tmt78GCIoIZgFI3emtK9keHYcGXK_r2bI3jUXl4P3_de8iHkERyQ5l0uA6w49SWJ3oIQYxZgShkPtgeoT1iEfcUjeYj6e6iHTpxbYoxlxPgx6hFOQkkV7iN_nNU2zcGzGZhPswDP1W4DKy_NvRyqslhAnlqvhEVa5O4UHSUmc3C2mwP0Mrp5Ht76k4fx3fB64luuGPeNsSy0giaxEDIx3FiIrZCMWBUzIWVsGWBDIVZK4LmChFgRJywMGzviBtMBuuj2rsviowK30avUWcgyk0NROS2IajJI-idIhFChFKQBZQfasnCuhESvy3RlyloTrNumeqnbXLrNpdum-qep3jbq-e5GNV9B_CvuIjbAVQd8pRnU_16sb-6n7a_x_c5Pm_LbvW_Kdx0JKrh-nY519DR8HNHZTE_pN_PBlFE</recordid><startdate>200405</startdate><enddate>200405</enddate><creator>Ichinohe, Akiko</creator><creator>Kure, Shigeo</creator><creator>Mikawa, Sumiko</creator><creator>Ueki, Takatoshi</creator><creator>Kojima, Kanako</creator><creator>Fujiwara, Kazuko</creator><creator>Iinuma, Kazuie</creator><creator>Matsubara, Yoichi</creator><creator>Sato, Kohji</creator><general>Blackwell Science Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>200405</creationdate><title>Glycine cleavage system in neurogenic regions</title><author>Ichinohe, Akiko ; 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Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of brain malformations. Although high levels of glycine have been considered to cause the above‐mentioned problems, the detailed pathogenesis of this disease is still unknown. Here we show that GCS is abundantly expressed in rat embryonic neural stem/progenitor cells in the neuroepithelium, and this expression is transmitted to the radial glia–astrocyte lineage, with prominence in postnatal neurogenic regions. These data indicate that GCS plays important roles in neurogenesis, and suggest that disturbance of neurogenesis induced by deficiency of GCS may be the main pathogenesis of nonketotic hyperglycinemia.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15128390</pmid><doi>10.1111/j.0953-816X.2004.03345.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acid Oxidoreductases - genetics Amino Acid Oxidoreductases - metabolism Amino Acid Transport System X-AG - genetics Amino Acid Transport System X-AG - metabolism Animals Animals, Newborn Brain - cytology Brain - physiology Brain Chemistry Carrier Proteins - genetics Carrier Proteins - metabolism Cells, Cultured Embryo, Mammalian Epithelial Cells - cytology Gene Expression Regulation, Developmental - physiology glycine glycine cleavage system Immunohistochemistry - methods Liver - enzymology Multienzyme Complexes - genetics Multienzyme Complexes - metabolism neural stem cell Neuroglia - enzymology Neurons - enzymology nonketotic hyperglycinemia rat Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - biosynthesis Transferases - genetics Transferases - metabolism |
| title | Glycine cleavage system in neurogenic regions |
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