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Investigation of SAMD1 ablation in mice
SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1 −/− and SAMD1 +/− mi...
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Published in: | Scientific reports 2023-02, Vol.13 (1), p.3000-3000, Article 3000 |
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description | SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1
−/−
and SAMD1
+/−
mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. In vitro, SAMD1 absence impaired neuronal differentiation processes. Heterozygous SAMD1 knockout mice underwent normal embryogenesis and were born alive. Postnatal genotyping showed a reduced ability of these mice to thrive, possibly due to altered steroidogenesis. In summary, the characterization of SAMD1 knockout mice suggests a critical role of SAMD1 during developmental processes in multiple organs and tissues. |
doi_str_mv | 10.1038/s41598-023-29779-3 |
format | article |
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−/−
and SAMD1
+/−
mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. In vitro, SAMD1 absence impaired neuronal differentiation processes. Heterozygous SAMD1 knockout mice underwent normal embryogenesis and were born alive. Postnatal genotyping showed a reduced ability of these mice to thrive, possibly due to altered steroidogenesis. In summary, the characterization of SAMD1 knockout mice suggests a critical role of SAMD1 during developmental processes in multiple organs and tissues.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-023-29779-3</identifier><identifier>PMID: 36810619</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136 ; 631/337/100 ; Animals ; Arteriosclerosis ; Blood vessels ; Chromatin ; Embryo, Mammalian - metabolism ; Embryogenesis ; Embryonic Development ; Embryonic growth stage ; Embryos ; Erythrocytes ; Gene regulation ; Genotyping ; Heterozygote ; Homozygote ; Humanities and Social Sciences ; Mice ; Mice, Knockout ; multidisciplinary ; Science ; Science (multidisciplinary) ; Steroidogenesis</subject><ispartof>Scientific reports, 2023-02, Vol.13 (1), p.3000-3000, Article 3000</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-6e1d697a6a229facddf1316960bf6b5dc7140a6fa5abbac6ac8a74b1ca560acf3</citedby><cites>FETCH-LOGICAL-c540t-6e1d697a6a229facddf1316960bf6b5dc7140a6fa5abbac6ac8a74b1ca560acf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2778492918/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2778492918?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36810619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Campbell, Bruce</creatorcontrib><creatorcontrib>Weber, Lisa M.</creatorcontrib><creatorcontrib>Engle, Sandra J.</creatorcontrib><creatorcontrib>Ozolinš, Terence R. S.</creatorcontrib><creatorcontrib>Bourassa, Patricia</creatorcontrib><creatorcontrib>Aiello, Robert</creatorcontrib><creatorcontrib>Liefke, Robert</creatorcontrib><title>Investigation of SAMD1 ablation in mice</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1
−/−
and SAMD1
+/−
mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. In vitro, SAMD1 absence impaired neuronal differentiation processes. Heterozygous SAMD1 knockout mice underwent normal embryogenesis and were born alive. Postnatal genotyping showed a reduced ability of these mice to thrive, possibly due to altered steroidogenesis. In summary, the characterization of SAMD1 knockout mice suggests a critical role of SAMD1 during developmental processes in multiple organs and tissues.</description><subject>631/136</subject><subject>631/337/100</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Blood vessels</subject><subject>Chromatin</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Embryogenesis</subject><subject>Embryonic Development</subject><subject>Embryonic growth stage</subject><subject>Embryos</subject><subject>Erythrocytes</subject><subject>Gene regulation</subject><subject>Genotyping</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humanities and Social Sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Steroidogenesis</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kc9PFTEQxxuiAQL8Ax7MSzzIZaG_t72YEFB5CcaDem6ms91nX_Ztsd1Hwn9vH4sIHuylzcx3PtOZLyFvGD1jVJjzIpmypqFcNNy2rW3EHjnkVKqGC85fPXsfkJNS1rQexa1kdp8cCG0Y1cwekvfL8S6UKa5gimlcpH7x7eLLFVuAH-ZIHBebiOGYvO5hKOHk8T4iPz59_H553dx8_by8vLhpUEk6NTqwTtsWNHBue8Cu65lg2mrqe-1Vhy2TFHQPCrwH1IAGWukZgtIUsBdHZDlzuwRrd5vjBvK9SxDdQyDllYM8RRyCs7wFj0YhopcaO8s5Rbkby3KGVFXWh5l1u_Wb0GEYpwzDC-jLzBh_ulW6c9ZKyVtWAaePgJx-beua3CYWDMMAY0jb4njdu5DaGFml7_6RrtM2j3VVO5WRlltmqorPKsyplBz6p88w6na2utlWV211D7Y6UYvePh_jqeSPiVUgZkGpqXEV8t_e_8H-BiJ-rCw</recordid><startdate>20230221</startdate><enddate>20230221</enddate><creator>Campbell, Bruce</creator><creator>Weber, Lisa M.</creator><creator>Engle, Sandra J.</creator><creator>Ozolinš, Terence R. 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S. ; Bourassa, Patricia ; Aiello, Robert ; Liefke, Robert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-6e1d697a6a229facddf1316960bf6b5dc7140a6fa5abbac6ac8a74b1ca560acf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>631/136</topic><topic>631/337/100</topic><topic>Animals</topic><topic>Arteriosclerosis</topic><topic>Blood vessels</topic><topic>Chromatin</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Embryogenesis</topic><topic>Embryonic Development</topic><topic>Embryonic growth stage</topic><topic>Embryos</topic><topic>Erythrocytes</topic><topic>Gene regulation</topic><topic>Genotyping</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Humanities and Social Sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Steroidogenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Campbell, Bruce</creatorcontrib><creatorcontrib>Weber, Lisa M.</creatorcontrib><creatorcontrib>Engle, Sandra J.</creatorcontrib><creatorcontrib>Ozolinš, Terence R. 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S.</au><au>Bourassa, Patricia</au><au>Aiello, Robert</au><au>Liefke, Robert</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of SAMD1 ablation in mice</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2023-02-21</date><risdate>2023</risdate><volume>13</volume><issue>1</issue><spage>3000</spage><epage>3000</epage><pages>3000-3000</pages><artnum>3000</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1
−/−
and SAMD1
+/−
mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. In vitro, SAMD1 absence impaired neuronal differentiation processes. Heterozygous SAMD1 knockout mice underwent normal embryogenesis and were born alive. Postnatal genotyping showed a reduced ability of these mice to thrive, possibly due to altered steroidogenesis. In summary, the characterization of SAMD1 knockout mice suggests a critical role of SAMD1 during developmental processes in multiple organs and tissues.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>36810619</pmid><doi>10.1038/s41598-023-29779-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/136 631/337/100 Animals Arteriosclerosis Blood vessels Chromatin Embryo, Mammalian - metabolism Embryogenesis Embryonic Development Embryonic growth stage Embryos Erythrocytes Gene regulation Genotyping Heterozygote Homozygote Humanities and Social Sciences Mice Mice, Knockout multidisciplinary Science Science (multidisciplinary) Steroidogenesis |
title | Investigation of SAMD1 ablation in mice |
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