A Polymorphic Form of Steroidogenic Factor-1 Is Associated with Adrenocorticotropin Resistance in Y1 Mouse Adrenocortical Tumor Cell Mutants
ACTH resistance in mutant derivatives of the Y1 mouse adrenocortical tumor cell line results from a defect that affects the activity of steroidogenic factor-1 (SF1), thereby preventing the expression of the melanocortin-2 receptor. In this report, we show that the SF1 genes in ACTH-resistant mutants...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2002-10, Vol.143 (10), p.4031-4037 |
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| description | ACTH resistance in mutant derivatives of the Y1 mouse adrenocortical tumor cell line results from a defect that affects the activity of steroidogenic factor-1 (SF1), thereby preventing the expression of the melanocortin-2 receptor. In this report, we show that the SF1 genes in ACTH-resistant mutants differ from the gene in ACTH-responsive Y1 cells by two base changes—one that changes an Ala to Ser at codon 172, and one in the third position of codon 3 that does not affect the protein sequence. Furthermore, several of the mutants contain multiple copies of this alternate SF1 gene (SF1S172) on acentric chromosome fragments. The SF1S172 allele represents a polymorphism rather than a spontaneous mutation because the two SF1 alleles can be traced to the hybrid mouse strain (C57L/J x A/HeJ) from which the original adrenal tumor was derived. The SF1A172 allele also is found in C57Bl/6J and C57Bl/10J mice, whereas the SF1S172 allele also is found in C3H/HeJ and DBA/2J mice. The two forms of SF1 had only modest differences in activity suggesting that the SF1 polymorphism per se is not directly responsible for ACTH resistance. Our results indicate that the SF1S172 allele is a marker of ACTH resistance in this family of adrenocortical tumor cells. |
| doi_str_mv | 10.1210/en.2002-220349 |
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In this report, we show that the SF1 genes in ACTH-resistant mutants differ from the gene in ACTH-responsive Y1 cells by two base changes—one that changes an Ala to Ser at codon 172, and one in the third position of codon 3 that does not affect the protein sequence. Furthermore, several of the mutants contain multiple copies of this alternate SF1 gene (SF1S172) on acentric chromosome fragments. The SF1S172 allele represents a polymorphism rather than a spontaneous mutation because the two SF1 alleles can be traced to the hybrid mouse strain (C57L/J x A/HeJ) from which the original adrenal tumor was derived. The SF1A172 allele also is found in C57Bl/6J and C57Bl/10J mice, whereas the SF1S172 allele also is found in C3H/HeJ and DBA/2J mice. The two forms of SF1 had only modest differences in activity suggesting that the SF1 polymorphism per se is not directly responsible for ACTH resistance. Our results indicate that the SF1S172 allele is a marker of ACTH resistance in this family of adrenocortical tumor cells.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2002-220349</identifier><identifier>PMID: 12239114</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Adrenal Cortex Neoplasms - genetics ; Adrenal Cortex Neoplasms - physiopathology ; Adrenocorticotropic hormone ; Adrenocorticotropic Hormone - pharmacology ; Adrenocorticotropin (ACTH) ; Alleles ; Amino acid sequence ; Animals ; Base Sequence - genetics ; Cells, Cultured ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Drug Resistance, Neoplasm - genetics ; Fushi Tarazu Transcription Factors ; Gene Amplification ; Homeodomain Proteins ; Melanocortin ; Mice ; Molecular Sequence Data ; Mutation - genetics ; Polymorphism ; Polymorphism, Genetic - physiology ; Receptors, Cytoplasmic and Nuclear ; Resistance factors ; Resistant mutant ; Species Specificity ; Steroidogenic Factor 1 ; Tissue Distribution ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcription, Genetic ; Tumor cell lines ; Tumor cells ; Tumors</subject><ispartof>Endocrinology (Philadelphia), 2002-10, Vol.143 (10), p.4031-4037</ispartof><rights>Copyright © 2002 by The Endocrine Society 2002</rights><rights>Copyright © 2002 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-d19fb8035daf767a54799683f7b72e080d6069c26c04567b55aa3d5475e96b103</citedby><cites>FETCH-LOGICAL-c439t-d19fb8035daf767a54799683f7b72e080d6069c26c04567b55aa3d5475e96b103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12239114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frigeri, Claudia</creatorcontrib><creatorcontrib>Tsao, Jennivine</creatorcontrib><creatorcontrib>Cordova, Martha</creatorcontrib><creatorcontrib>Schimmer, Bernard P</creatorcontrib><title>A Polymorphic Form of Steroidogenic Factor-1 Is Associated with Adrenocorticotropin Resistance in Y1 Mouse Adrenocortical Tumor Cell Mutants</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>ACTH resistance in mutant derivatives of the Y1 mouse adrenocortical tumor cell line results from a defect that affects the activity of steroidogenic factor-1 (SF1), thereby preventing the expression of the melanocortin-2 receptor. In this report, we show that the SF1 genes in ACTH-resistant mutants differ from the gene in ACTH-responsive Y1 cells by two base changes—one that changes an Ala to Ser at codon 172, and one in the third position of codon 3 that does not affect the protein sequence. Furthermore, several of the mutants contain multiple copies of this alternate SF1 gene (SF1S172) on acentric chromosome fragments. The SF1S172 allele represents a polymorphism rather than a spontaneous mutation because the two SF1 alleles can be traced to the hybrid mouse strain (C57L/J x A/HeJ) from which the original adrenal tumor was derived. The SF1A172 allele also is found in C57Bl/6J and C57Bl/10J mice, whereas the SF1S172 allele also is found in C3H/HeJ and DBA/2J mice. The two forms of SF1 had only modest differences in activity suggesting that the SF1 polymorphism per se is not directly responsible for ACTH resistance. Our results indicate that the SF1S172 allele is a marker of ACTH resistance in this family of adrenocortical tumor cells.</description><subject>Adrenal Cortex Neoplasms - genetics</subject><subject>Adrenal Cortex Neoplasms - physiopathology</subject><subject>Adrenocorticotropic hormone</subject><subject>Adrenocorticotropic Hormone - pharmacology</subject><subject>Adrenocorticotropin (ACTH)</subject><subject>Alleles</subject><subject>Amino acid sequence</subject><subject>Animals</subject><subject>Base Sequence - genetics</subject><subject>Cells, Cultured</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Fushi Tarazu Transcription Factors</subject><subject>Gene Amplification</subject><subject>Homeodomain Proteins</subject><subject>Melanocortin</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Mutation - genetics</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic - physiology</subject><subject>Receptors, Cytoplasmic and Nuclear</subject><subject>Resistance factors</subject><subject>Resistant mutant</subject><subject>Species Specificity</subject><subject>Steroidogenic Factor 1</subject><subject>Tissue Distribution</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><subject>Tumor cell lines</subject><subject>Tumor cells</subject><subject>Tumors</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9rFDEYh4Modq1ePUpAEDzMNv9msjkui7WFFovWg6chk7xjU2aSMckg_Q5-6GaZpcVCT-ENT355eH8IvadkTRklJ-DXjBBWMUa4UC_QiipRV5JK8hKtCKG8kozJI_QmpdsyCiH4a3REGeOKUrFC_7b4Kgx3Y4jTjTP4NMQRhx7_yBCDs-E3-P2tNjnEiuLzhLcpBeN0Bov_unyDtzaCDybE7EzIMUzO4--QXMraG8Bl-kXxZZgT_IfqAV_P5Ve8g2HAl3Ohc3qLXvV6SPDucB6jn6dfrndn1cW3r-e77UVlBFe5slT13Ybw2upeNlLXQirVbHgvO8mAbIhtSKMMawwRdSO7utaa20LVoJqOEn6MPi25Uwx_Zki5HV0yRUR7KKatLJuVRDUF_PgEvA1z9MWt5ZSTmivCZaHWC2ViSClC307RjTretZS0-5Za8O2-pXZpqTz4cIiduxHsI36opQCfFyDM03Nh1UNYvbDgbTDReZgipPRo-ozEPd3NquM</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>Frigeri, Claudia</creator><creator>Tsao, Jennivine</creator><creator>Cordova, Martha</creator><creator>Schimmer, Bernard P</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200210</creationdate><title>A Polymorphic Form of Steroidogenic Factor-1 Is Associated with Adrenocorticotropin Resistance in Y1 Mouse Adrenocortical Tumor Cell Mutants</title><author>Frigeri, Claudia ; Tsao, Jennivine ; Cordova, Martha ; Schimmer, Bernard P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-d19fb8035daf767a54799683f7b72e080d6069c26c04567b55aa3d5475e96b103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adrenal Cortex Neoplasms - genetics</topic><topic>Adrenal Cortex Neoplasms - physiopathology</topic><topic>Adrenocorticotropic hormone</topic><topic>Adrenocorticotropic Hormone - pharmacology</topic><topic>Adrenocorticotropin (ACTH)</topic><topic>Alleles</topic><topic>Amino acid sequence</topic><topic>Animals</topic><topic>Base Sequence - genetics</topic><topic>Cells, Cultured</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Fushi Tarazu Transcription Factors</topic><topic>Gene Amplification</topic><topic>Homeodomain Proteins</topic><topic>Melanocortin</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Mutation - genetics</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic - physiology</topic><topic>Receptors, Cytoplasmic and Nuclear</topic><topic>Resistance factors</topic><topic>Resistant mutant</topic><topic>Species Specificity</topic><topic>Steroidogenic Factor 1</topic><topic>Tissue Distribution</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic</topic><topic>Tumor cell lines</topic><topic>Tumor cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frigeri, Claudia</creatorcontrib><creatorcontrib>Tsao, Jennivine</creatorcontrib><creatorcontrib>Cordova, Martha</creatorcontrib><creatorcontrib>Schimmer, Bernard P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frigeri, Claudia</au><au>Tsao, Jennivine</au><au>Cordova, Martha</au><au>Schimmer, Bernard P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Polymorphic Form of Steroidogenic Factor-1 Is Associated with Adrenocorticotropin Resistance in Y1 Mouse Adrenocortical Tumor Cell Mutants</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2002-10</date><risdate>2002</risdate><volume>143</volume><issue>10</issue><spage>4031</spage><epage>4037</epage><pages>4031-4037</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>ACTH resistance in mutant derivatives of the Y1 mouse adrenocortical tumor cell line results from a defect that affects the activity of steroidogenic factor-1 (SF1), thereby preventing the expression of the melanocortin-2 receptor. In this report, we show that the SF1 genes in ACTH-resistant mutants differ from the gene in ACTH-responsive Y1 cells by two base changes—one that changes an Ala to Ser at codon 172, and one in the third position of codon 3 that does not affect the protein sequence. Furthermore, several of the mutants contain multiple copies of this alternate SF1 gene (SF1S172) on acentric chromosome fragments. The SF1S172 allele represents a polymorphism rather than a spontaneous mutation because the two SF1 alleles can be traced to the hybrid mouse strain (C57L/J x A/HeJ) from which the original adrenal tumor was derived. The SF1A172 allele also is found in C57Bl/6J and C57Bl/10J mice, whereas the SF1S172 allele also is found in C3H/HeJ and DBA/2J mice. The two forms of SF1 had only modest differences in activity suggesting that the SF1 polymorphism per se is not directly responsible for ACTH resistance. Our results indicate that the SF1S172 allele is a marker of ACTH resistance in this family of adrenocortical tumor cells.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>12239114</pmid><doi>10.1210/en.2002-220349</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals |
| subjects | Adrenal Cortex Neoplasms - genetics Adrenal Cortex Neoplasms - physiopathology Adrenocorticotropic hormone Adrenocorticotropic Hormone - pharmacology Adrenocorticotropin (ACTH) Alleles Amino acid sequence Animals Base Sequence - genetics Cells, Cultured DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Drug Resistance, Neoplasm - genetics Fushi Tarazu Transcription Factors Gene Amplification Homeodomain Proteins Melanocortin Mice Molecular Sequence Data Mutation - genetics Polymorphism Polymorphism, Genetic - physiology Receptors, Cytoplasmic and Nuclear Resistance factors Resistant mutant Species Specificity Steroidogenic Factor 1 Tissue Distribution Transcription Factors - genetics Transcription Factors - metabolism Transcription, Genetic Tumor cell lines Tumor cells Tumors |
| title | A Polymorphic Form of Steroidogenic Factor-1 Is Associated with Adrenocorticotropin Resistance in Y1 Mouse Adrenocortical Tumor Cell Mutants |
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