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New insights into SRY regulation through identification of 5' conserved sequences

BACKGROUND: SRY is the pivotal gene initiating male sex determination in most mammals, but how its expression is regulated is still not understood. In this study we derived novel SRY 5' flanking genomic sequence data from bovine and caprine genomic BAC clones. RESULTS: We identified four interv...

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Detalles Bibliográficos
Autores principales: Ross, Diana GF, Bowles, Josephine, Koopman, Peter, Lehnert, Sigrid
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2572636/
https://www.ncbi.nlm.nih.gov/pubmed/18851760
http://dx.doi.org/10.1186/1471-2199-9-85
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author Ross, Diana GF
Bowles, Josephine
Koopman, Peter
Lehnert, Sigrid
author_facet Ross, Diana GF
Bowles, Josephine
Koopman, Peter
Lehnert, Sigrid
author_sort Ross, Diana GF
collection PubMed
description BACKGROUND: SRY is the pivotal gene initiating male sex determination in most mammals, but how its expression is regulated is still not understood. In this study we derived novel SRY 5' flanking genomic sequence data from bovine and caprine genomic BAC clones. RESULTS: We identified four intervals of high homology upstream of SRY by comparison of human, bovine, pig, goat and mouse genomic sequences. These conserved regions contain putative binding sites for a large number of known transcription factor families, including several that have been implicated previously in sex determination and early gonadal development. CONCLUSION: Our results reveal potentially important SRY regulatory elements, mutations in which might underlie cases of idiopathic human XY sex reversal.
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spelling pubmed-25726362008-10-25 New insights into SRY regulation through identification of 5' conserved sequences Ross, Diana GF Bowles, Josephine Koopman, Peter Lehnert, Sigrid BMC Mol Biol Research Article BACKGROUND: SRY is the pivotal gene initiating male sex determination in most mammals, but how its expression is regulated is still not understood. In this study we derived novel SRY 5' flanking genomic sequence data from bovine and caprine genomic BAC clones. RESULTS: We identified four intervals of high homology upstream of SRY by comparison of human, bovine, pig, goat and mouse genomic sequences. These conserved regions contain putative binding sites for a large number of known transcription factor families, including several that have been implicated previously in sex determination and early gonadal development. CONCLUSION: Our results reveal potentially important SRY regulatory elements, mutations in which might underlie cases of idiopathic human XY sex reversal. BioMed Central 2008-10-14 /pmc/articles/PMC2572636/ /pubmed/18851760 http://dx.doi.org/10.1186/1471-2199-9-85 Text en Copyright © 2008 Ross et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Ross, Diana GF
Bowles, Josephine
Koopman, Peter
Lehnert, Sigrid
New insights into SRY regulation through identification of 5' conserved sequences
title New insights into SRY regulation through identification of 5' conserved sequences
title_full New insights into SRY regulation through identification of 5' conserved sequences
title_fullStr New insights into SRY regulation through identification of 5' conserved sequences
title_full_unstemmed New insights into SRY regulation through identification of 5' conserved sequences
title_short New insights into SRY regulation through identification of 5' conserved sequences
title_sort new insights into sry regulation through identification of 5' conserved sequences
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2572636/
https://www.ncbi.nlm.nih.gov/pubmed/18851760
http://dx.doi.org/10.1186/1471-2199-9-85
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