Abnormalities of developmental cell death in Dad1‐deficient mice
Background Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21‐derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl‐2. Results To determine the role of Dad1 function i...
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| Veröffentlicht in: | Genes to cells : devoted to molecular & cellular mechanisms 1999-04, Vol.4 (4), p.243-252 |
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| container_title | Genes to cells : devoted to molecular & cellular mechanisms |
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| creator | Nishii, Kiyomasa Tsuzuki, Teruhisa Kumai, Madoka Takeda, Naoki Koga, Hideya Aizawa, Shinichi Nishimoto, Takeharu Shibata, Yosaburo |
| description | Background
Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21‐derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl‐2.
Results
To determine the role of Dad1 function in vivo, we prepared by gene targeting, mice harbouring a disrupted Dad1 gene. Homozygous mutants died shortly after they were implanted with the characteristic features of apoptosis. In an in vitro blastocyst culture system, Dad1‐null cells displayed abnormalities which were comparable to those obtained in vivo. However, oligosaccharyltransferase activity was apparently retained even after the Dad1‐null cells were destined to die. Some live‐born heterozygous mutants displayed soft‐tissue syndactyly. Mild thymic hypoplasia was also indicated in heterozygotes.
Conclusion
These results suggest the involvement of the Dad1 gene in the acquisition of a common syndactyly phenotype, as well as in the control of programmed cell death during development. |
| doi_str_mv | 10.1046/j.1365-2443.1999.00256.x |
| format | Article |
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Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21‐derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl‐2.
Results
To determine the role of Dad1 function in vivo, we prepared by gene targeting, mice harbouring a disrupted Dad1 gene. Homozygous mutants died shortly after they were implanted with the characteristic features of apoptosis. In an in vitro blastocyst culture system, Dad1‐null cells displayed abnormalities which were comparable to those obtained in vivo. However, oligosaccharyltransferase activity was apparently retained even after the Dad1‐null cells were destined to die. Some live‐born heterozygous mutants displayed soft‐tissue syndactyly. Mild thymic hypoplasia was also indicated in heterozygotes.
Conclusion
These results suggest the involvement of the Dad1 gene in the acquisition of a common syndactyly phenotype, as well as in the control of programmed cell death during development.</description><identifier>ISSN: 1356-9597</identifier><identifier>EISSN: 1365-2443</identifier><identifier>DOI: 10.1046/j.1365-2443.1999.00256.x</identifier><identifier>PMID: 10336695</identifier><language>eng</language><publisher>Oxford BSL: Blackwell Science Ltd</publisher><subject>Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; Blastocyst - physiology ; Cells, Cultured ; Crosses, Genetic ; Embryonic and Fetal Development ; Extremities - embryology ; Female ; Gene Deletion ; Gene Targeting ; Hexosyltransferases ; Male ; Membrane Proteins - deficiency ; Membrane Proteins - genetics ; Membrane Proteins - physiology ; Mice ; Syndactyly - genetics ; Thymus Gland - pathology ; Transferases - metabolism</subject><ispartof>Genes to cells : devoted to molecular & cellular mechanisms, 1999-04, Vol.4 (4), p.243-252</ispartof><rights>Blackwell Science Ltd, Oxford</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5116-a58839761e6463c35ac8d8a08d14b7ed50186e96ca539c31bdf900b8265021f03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2443.1999.00256.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2443.1999.00256.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10336695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishii, Kiyomasa</creatorcontrib><creatorcontrib>Tsuzuki, Teruhisa</creatorcontrib><creatorcontrib>Kumai, Madoka</creatorcontrib><creatorcontrib>Takeda, Naoki</creatorcontrib><creatorcontrib>Koga, Hideya</creatorcontrib><creatorcontrib>Aizawa, Shinichi</creatorcontrib><creatorcontrib>Nishimoto, Takeharu</creatorcontrib><creatorcontrib>Shibata, Yosaburo</creatorcontrib><title>Abnormalities of developmental cell death in Dad1‐deficient mice</title><title>Genes to cells : devoted to molecular & cellular mechanisms</title><addtitle>Genes Cells</addtitle><description>Background
Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21‐derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl‐2.
Results
To determine the role of Dad1 function in vivo, we prepared by gene targeting, mice harbouring a disrupted Dad1 gene. Homozygous mutants died shortly after they were implanted with the characteristic features of apoptosis. In an in vitro blastocyst culture system, Dad1‐null cells displayed abnormalities which were comparable to those obtained in vivo. However, oligosaccharyltransferase activity was apparently retained even after the Dad1‐null cells were destined to die. Some live‐born heterozygous mutants displayed soft‐tissue syndactyly. Mild thymic hypoplasia was also indicated in heterozygotes.
Conclusion
These results suggest the involvement of the Dad1 gene in the acquisition of a common syndactyly phenotype, as well as in the control of programmed cell death during development.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Blastocyst - physiology</subject><subject>Cells, Cultured</subject><subject>Crosses, Genetic</subject><subject>Embryonic and Fetal Development</subject><subject>Extremities - embryology</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Gene Targeting</subject><subject>Hexosyltransferases</subject><subject>Male</subject><subject>Membrane Proteins - deficiency</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - physiology</subject><subject>Mice</subject><subject>Syndactyly - genetics</subject><subject>Thymus Gland - pathology</subject><subject>Transferases - metabolism</subject><issn>1356-9597</issn><issn>1365-2443</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtOwzAQQC0EoqVwBZQVu4RxHDu2xKYUKEiV2JS15diOcJVPiVNodxyBM3ISElIhdrCa0cybjx5CAYYIQ8IuVxEmjIZxkpAICyEigJiyaHuAxj-Nwz6nLBRUpCN04v0KAJMY6DEaYSCEMUHH6HqaVXVTqsK1zvqgzgNjX21Rr0tbtaoItC2KrqTa58BVwY0y-PP9w9jcadcBQem0PUVHuSq8PdvHCXq6u13O7sPF4_xhNl2EmmLMQkU5JyJl2LKEEU2o0txwBdzgJEutoYA5s4JpRYnQBGcmFwAZjxmFGOdAJuhi2Ltu6peN9a0sne__U5WtN14ykaaCQPoniNOYpQlJOpAPoG5q7xuby3XjStXsJAbZi5Yr2fuUvU_Zi5bfouW2Gz3f39hkpTW_BgezHXA1AG-usLt_L5bz5axLyBfIBos0</recordid><startdate>199904</startdate><enddate>199904</enddate><creator>Nishii, Kiyomasa</creator><creator>Tsuzuki, Teruhisa</creator><creator>Kumai, Madoka</creator><creator>Takeda, Naoki</creator><creator>Koga, Hideya</creator><creator>Aizawa, Shinichi</creator><creator>Nishimoto, Takeharu</creator><creator>Shibata, Yosaburo</creator><general>Blackwell Science Ltd</general><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>199904</creationdate><title>Abnormalities of developmental cell death in Dad1‐deficient mice</title><author>Nishii, Kiyomasa ; Tsuzuki, Teruhisa ; Kumai, Madoka ; Takeda, Naoki ; Koga, Hideya ; Aizawa, Shinichi ; Nishimoto, Takeharu ; Shibata, Yosaburo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5116-a58839761e6463c35ac8d8a08d14b7ed50186e96ca539c31bdf900b8265021f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Blastocyst - physiology</topic><topic>Cells, Cultured</topic><topic>Crosses, Genetic</topic><topic>Embryonic and Fetal Development</topic><topic>Extremities - embryology</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Gene Targeting</topic><topic>Hexosyltransferases</topic><topic>Male</topic><topic>Membrane Proteins - deficiency</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - physiology</topic><topic>Mice</topic><topic>Syndactyly - genetics</topic><topic>Thymus Gland - pathology</topic><topic>Transferases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishii, Kiyomasa</creatorcontrib><creatorcontrib>Tsuzuki, Teruhisa</creatorcontrib><creatorcontrib>Kumai, Madoka</creatorcontrib><creatorcontrib>Takeda, Naoki</creatorcontrib><creatorcontrib>Koga, Hideya</creatorcontrib><creatorcontrib>Aizawa, Shinichi</creatorcontrib><creatorcontrib>Nishimoto, Takeharu</creatorcontrib><creatorcontrib>Shibata, Yosaburo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishii, Kiyomasa</au><au>Tsuzuki, Teruhisa</au><au>Kumai, Madoka</au><au>Takeda, Naoki</au><au>Koga, Hideya</au><au>Aizawa, Shinichi</au><au>Nishimoto, Takeharu</au><au>Shibata, Yosaburo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormalities of developmental cell death in Dad1‐deficient mice</atitle><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle><addtitle>Genes Cells</addtitle><date>1999-04</date><risdate>1999</risdate><volume>4</volume><issue>4</issue><spage>243</spage><epage>252</epage><pages>243-252</pages><issn>1356-9597</issn><eissn>1365-2443</eissn><abstract>Background
Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21‐derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl‐2.
Results
To determine the role of Dad1 function in vivo, we prepared by gene targeting, mice harbouring a disrupted Dad1 gene. Homozygous mutants died shortly after they were implanted with the characteristic features of apoptosis. In an in vitro blastocyst culture system, Dad1‐null cells displayed abnormalities which were comparable to those obtained in vivo. However, oligosaccharyltransferase activity was apparently retained even after the Dad1‐null cells were destined to die. Some live‐born heterozygous mutants displayed soft‐tissue syndactyly. Mild thymic hypoplasia was also indicated in heterozygotes.
Conclusion
These results suggest the involvement of the Dad1 gene in the acquisition of a common syndactyly phenotype, as well as in the control of programmed cell death during development.</abstract><cop>Oxford BSL</cop><pub>Blackwell Science Ltd</pub><pmid>10336695</pmid><doi>10.1046/j.1365-2443.1999.00256.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Free Content; Freely Accessible Japanese Titles; EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals |
| subjects | Animals Apoptosis Apoptosis Regulatory Proteins Blastocyst - physiology Cells, Cultured Crosses, Genetic Embryonic and Fetal Development Extremities - embryology Female Gene Deletion Gene Targeting Hexosyltransferases Male Membrane Proteins - deficiency Membrane Proteins - genetics Membrane Proteins - physiology Mice Syndactyly - genetics Thymus Gland - pathology Transferases - metabolism |
| title | Abnormalities of developmental cell death in Dad1‐deficient mice |
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