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Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice

BACKGROUND: The A(y) allele at the agouti locus causes obesity and promotes linear growth in mice. The effect of the A(y) allele on obesity has been extensively investigated, whereas its effect on body length is only poorly analyzed. To gain insight into the genetic control of body length, quantitat...

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Autor principal: Suto, Jun-ichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517383/
https://www.ncbi.nlm.nih.gov/pubmed/23031221
http://dx.doi.org/10.1186/1756-0500-5-547
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author Suto, Jun-ichi
author_facet Suto, Jun-ichi
author_sort Suto, Jun-ichi
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description BACKGROUND: The A(y) allele at the agouti locus causes obesity and promotes linear growth in mice. The effect of the A(y) allele on obesity has been extensively investigated, whereas its effect on body length is only poorly analyzed. To gain insight into the genetic control of body length, quantitative trait locus (QTL) analysis was performed in F(2) female mice produced by crossing C57BL/6 J females and DDD.Cg-A(y) males. A congenic DDD.Cg-A(y) strain was established by introgressing the A(y) allele from the B6.Cg-A(y) strain by backcrossing for 12 generations. DDD.Cg-A(y) females were longer than B6.Cg-A(y) females; therefore, QTLs that interact with the A(y) allele may be identified for body length. In addition, QTL analysis was also performed for plasma insulin-like growth factor 1 (IGF1) levels because IGF1 is known to play essential roles in growth and development. If QTLs for IGF1 levels coincide with those for body length, we can gain endocrinological insight into the QTLs for body length. RESULTS: Correlations between body length and IGF1 levels were statistically significant in F(2) populations. For body length, two significant QTLs were identified on chromosomes 15 and 17. For IGF1 levels, three significant QTLs were identified on chromosomes 10, 12, and 19. QTLs on chromosomes 12 and 19 appeared to be novel, and the latter interacted with the A(y) allele. CONCLUSION: QTLs for body length and IGF1 levels contained candidate genes that were components of the growth hormone/insulin-like growth factor axis. However, there was no overlap between QTLs for these two traits. Contrary to our expectations, QTLs that interacted with the A(y) allele were identified not for body length but for IGF1 levels. Body length and IGF1 levels were, thus, controlled by different sets of genes.
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spelling pubmed-35173832012-12-08 Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice Suto, Jun-ichi BMC Res Notes Research Article BACKGROUND: The A(y) allele at the agouti locus causes obesity and promotes linear growth in mice. The effect of the A(y) allele on obesity has been extensively investigated, whereas its effect on body length is only poorly analyzed. To gain insight into the genetic control of body length, quantitative trait locus (QTL) analysis was performed in F(2) female mice produced by crossing C57BL/6 J females and DDD.Cg-A(y) males. A congenic DDD.Cg-A(y) strain was established by introgressing the A(y) allele from the B6.Cg-A(y) strain by backcrossing for 12 generations. DDD.Cg-A(y) females were longer than B6.Cg-A(y) females; therefore, QTLs that interact with the A(y) allele may be identified for body length. In addition, QTL analysis was also performed for plasma insulin-like growth factor 1 (IGF1) levels because IGF1 is known to play essential roles in growth and development. If QTLs for IGF1 levels coincide with those for body length, we can gain endocrinological insight into the QTLs for body length. RESULTS: Correlations between body length and IGF1 levels were statistically significant in F(2) populations. For body length, two significant QTLs were identified on chromosomes 15 and 17. For IGF1 levels, three significant QTLs were identified on chromosomes 10, 12, and 19. QTLs on chromosomes 12 and 19 appeared to be novel, and the latter interacted with the A(y) allele. CONCLUSION: QTLs for body length and IGF1 levels contained candidate genes that were components of the growth hormone/insulin-like growth factor axis. However, there was no overlap between QTLs for these two traits. Contrary to our expectations, QTLs that interacted with the A(y) allele were identified not for body length but for IGF1 levels. Body length and IGF1 levels were, thus, controlled by different sets of genes. BioMed Central 2012-10-02 /pmc/articles/PMC3517383/ /pubmed/23031221 http://dx.doi.org/10.1186/1756-0500-5-547 Text en Copyright ©2012 Suto; 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
Suto, Jun-ichi
Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title_full Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title_fullStr Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title_full_unstemmed Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title_short Quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
title_sort quantitative trait locus mapping of genes that control body length and plasma insulin-like growth factor 1 level in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517383/
https://www.ncbi.nlm.nih.gov/pubmed/23031221
http://dx.doi.org/10.1186/1756-0500-5-547
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