Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2
Proteins containing the ARID (AT-rich interaction domain) DNA-binding motif regulate gene expression and differentiation in fungi, plants, and animals. This report describes phenotypes resulting from targeted disruption of the ARID gene Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neon...
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Veröffentlicht in: | Biochemical and biophysical research communications 2003-12, Vol.312 (4), p.997-1004 |
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creator | Whitson, Robert H Tsark, Walter Huang, Ting H Itakura, Keiichi |
description | Proteins containing the ARID (AT-rich interaction domain) DNA-binding motif regulate gene expression and differentiation in fungi, plants, and animals. This report describes phenotypes resulting from targeted disruption of the ARID gene
Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neonatal mortality that was partially strain-dependent: survival of
Mrf-2
−/− pups ranged from 6.4% on the 129S1 genetic background to 38% on a mixed 129S1·C57Bl/6J background. Loss of Mrf-2 expression did not affect embryonic survival, embryonic growth or birth weight. Lipid accumulation was severely reduced in brown adipose of
Mrf-2
−/− neonates at 24
h of age, however, and
Mrf-2
−/− mice weighed significantly less than controls from postnatal day five onward. Adult
Mrf-2
−/− mice were lean, with significant reductions in brown and white adipose tissues, and in the percentage of body fat.
Mrf-2
−/− and
Mrf-2
+/− mice were also resistant to weight gains and obesity when maintained on high-fat diets. These phenotypes suggest that Mrf-2 is essential for accumulation of lipid stores in postnatal life. |
doi_str_mv | 10.1016/j.bbrc.2003.11.026 |
format | Article |
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Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neonatal mortality that was partially strain-dependent: survival of
Mrf-2
−/− pups ranged from 6.4% on the 129S1 genetic background to 38% on a mixed 129S1·C57Bl/6J background. Loss of Mrf-2 expression did not affect embryonic survival, embryonic growth or birth weight. Lipid accumulation was severely reduced in brown adipose of
Mrf-2
−/− neonates at 24
h of age, however, and
Mrf-2
−/− mice weighed significantly less than controls from postnatal day five onward. Adult
Mrf-2
−/− mice were lean, with significant reductions in brown and white adipose tissues, and in the percentage of body fat.
Mrf-2
−/− and
Mrf-2
+/− mice were also resistant to weight gains and obesity when maintained on high-fat diets. These phenotypes suggest that Mrf-2 is essential for accumulation of lipid stores in postnatal life.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2003.11.026</identifier><identifier>PMID: 14651970</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Aging - physiology ; Animals ; Animals, Newborn ; AT-rich interaction domain ; Body Constitution - physiology ; Body Weight - physiology ; Brown adipose tissue ; Diet-induced obesity ; Dietary Fats - metabolism ; DNA-Binding Proteins - deficiency ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Leanness ; Mice ; Mice, Inbred C57BL ; Mrf-2 protein ; Myogenic Regulatory Factors - genetics ; Neonatal mortality ; Phenotype ; Sex Factors ; Structure-Activity Relationship ; Survival Rate ; Thinness - genetics ; Thinness - metabolism ; Transcription Factors ; White adipose tissue</subject><ispartof>Biochemical and biophysical research communications, 2003-12, Vol.312 (4), p.997-1004</ispartof><rights>2003 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-76f8026498f6fe4944d4a857019c01421952c1470ce20a91b88c60a401e55cbc3</citedby><cites>FETCH-LOGICAL-c449t-76f8026498f6fe4944d4a857019c01421952c1470ce20a91b88c60a401e55cbc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X03023763$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14651970$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Whitson, Robert H</creatorcontrib><creatorcontrib>Tsark, Walter</creatorcontrib><creatorcontrib>Huang, Ting H</creatorcontrib><creatorcontrib>Itakura, Keiichi</creatorcontrib><title>Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Proteins containing the ARID (AT-rich interaction domain) DNA-binding motif regulate gene expression and differentiation in fungi, plants, and animals. This report describes phenotypes resulting from targeted disruption of the ARID gene
Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neonatal mortality that was partially strain-dependent: survival of
Mrf-2
−/− pups ranged from 6.4% on the 129S1 genetic background to 38% on a mixed 129S1·C57Bl/6J background. Loss of Mrf-2 expression did not affect embryonic survival, embryonic growth or birth weight. Lipid accumulation was severely reduced in brown adipose of
Mrf-2
−/− neonates at 24
h of age, however, and
Mrf-2
−/− mice weighed significantly less than controls from postnatal day five onward. Adult
Mrf-2
−/− mice were lean, with significant reductions in brown and white adipose tissues, and in the percentage of body fat.
Mrf-2
−/− and
Mrf-2
+/− mice were also resistant to weight gains and obesity when maintained on high-fat diets. These phenotypes suggest that Mrf-2 is essential for accumulation of lipid stores in postnatal life.</description><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>AT-rich interaction domain</subject><subject>Body Constitution - physiology</subject><subject>Body Weight - physiology</subject><subject>Brown adipose tissue</subject><subject>Diet-induced obesity</subject><subject>Dietary Fats - metabolism</subject><subject>DNA-Binding Proteins - deficiency</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Leanness</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mrf-2 protein</subject><subject>Myogenic Regulatory Factors - genetics</subject><subject>Neonatal mortality</subject><subject>Phenotype</subject><subject>Sex Factors</subject><subject>Structure-Activity Relationship</subject><subject>Survival Rate</subject><subject>Thinness - genetics</subject><subject>Thinness - metabolism</subject><subject>Transcription Factors</subject><subject>White adipose tissue</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAURS1ERYeWP8ACecUu6Xsex4klNlX5qtQWCYrEznKcF_CQOIPtQeq_x6MZiV27upvzru47jL1GqBFQXWzqvo-uFgDrGrEGoZ6xFYKGSiDI52wFAKoSGn-cspcpbQAQpdIv2GmJBnULK_btjpZgs534vMQSPj9wGwY-kQ2BUuI-8Nk74pN1v334yfMv4pdfr9_zHG1ILvpt9kvgo3V5ifw2jpU4ZyejnRK9OuYZ-_7xw_3V5-rmy6frq8ubykmpc9WqsSubpe5GNZLUUg7Sdk0LqB2gFKgb4VC24EiA1dh3nVNgJSA1jevd-oy9PfRu4_JnRymb2SdH02QDLbtk2vKmFBKfBFGLRqFaF1AcQBeXlCKNZhv9bOODQTB752Zj9s7N3rlBNGV_OXpzbN_1Mw3_T46SC_DuAFCR8ddTNMl5Co4GH8llMyz-sf5_vI-Qiw</recordid><startdate>20031226</startdate><enddate>20031226</enddate><creator>Whitson, Robert H</creator><creator>Tsark, Walter</creator><creator>Huang, Ting H</creator><creator>Itakura, Keiichi</creator><general>Elsevier Inc</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>20031226</creationdate><title>Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2</title><author>Whitson, Robert H ; Tsark, Walter ; Huang, Ting H ; Itakura, Keiichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-76f8026498f6fe4944d4a857019c01421952c1470ce20a91b88c60a401e55cbc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - pathology</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>AT-rich interaction domain</topic><topic>Body Constitution - physiology</topic><topic>Body Weight - physiology</topic><topic>Brown adipose tissue</topic><topic>Diet-induced obesity</topic><topic>Dietary Fats - metabolism</topic><topic>DNA-Binding Proteins - deficiency</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Leanness</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mrf-2 protein</topic><topic>Myogenic Regulatory Factors - genetics</topic><topic>Neonatal mortality</topic><topic>Phenotype</topic><topic>Sex Factors</topic><topic>Structure-Activity Relationship</topic><topic>Survival Rate</topic><topic>Thinness - genetics</topic><topic>Thinness - metabolism</topic><topic>Transcription Factors</topic><topic>White adipose tissue</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Whitson, Robert H</creatorcontrib><creatorcontrib>Tsark, Walter</creatorcontrib><creatorcontrib>Huang, Ting H</creatorcontrib><creatorcontrib>Itakura, Keiichi</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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Whitson, Robert H</au><au>Tsark, Walter</au><au>Huang, Ting H</au><au>Itakura, Keiichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003-12-26</date><risdate>2003</risdate><volume>312</volume><issue>4</issue><spage>997</spage><epage>1004</epage><pages>997-1004</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Proteins containing the ARID (AT-rich interaction domain) DNA-binding motif regulate gene expression and differentiation in fungi, plants, and animals. This report describes phenotypes resulting from targeted disruption of the ARID gene
Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neonatal mortality that was partially strain-dependent: survival of
Mrf-2
−/− pups ranged from 6.4% on the 129S1 genetic background to 38% on a mixed 129S1·C57Bl/6J background. Loss of Mrf-2 expression did not affect embryonic survival, embryonic growth or birth weight. Lipid accumulation was severely reduced in brown adipose of
Mrf-2
−/− neonates at 24
h of age, however, and
Mrf-2
−/− mice weighed significantly less than controls from postnatal day five onward. Adult
Mrf-2
−/− mice were lean, with significant reductions in brown and white adipose tissues, and in the percentage of body fat.
Mrf-2
−/− and
Mrf-2
+/− mice were also resistant to weight gains and obesity when maintained on high-fat diets. These phenotypes suggest that Mrf-2 is essential for accumulation of lipid stores in postnatal life.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>14651970</pmid><doi>10.1016/j.bbrc.2003.11.026</doi><tpages>8</tpages></addata></record> |
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subjects | Adipose Tissue - metabolism Adipose Tissue - pathology Aging - physiology Animals Animals, Newborn AT-rich interaction domain Body Constitution - physiology Body Weight - physiology Brown adipose tissue Diet-induced obesity Dietary Fats - metabolism DNA-Binding Proteins - deficiency DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Leanness Mice Mice, Inbred C57BL Mrf-2 protein Myogenic Regulatory Factors - genetics Neonatal mortality Phenotype Sex Factors Structure-Activity Relationship Survival Rate Thinness - genetics Thinness - metabolism Transcription Factors White adipose tissue |
title | Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2 |
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