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Lisbeth Schmidt Laursen

Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish

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Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish. / Kamei, Hiroyasu; Lu, Ling; Jiao, Shuang; Li, Yun; Nielsen, Claus Gyrup; Laursen, Lisbeth Schmidt; Oxvig, Claus; Zhou, Jianfeng; Duan, Cunming.

In: P L o S One, Vol. 3, No. 8, 12.2008, p. e3091.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Kamei, H, Lu, L, Jiao, S, Li, Y, Nielsen, CG, Laursen, LS, Oxvig, C, Zhou, J & Duan, C 2008, 'Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish', P L o S One, vol. 3, no. 8, pp. e3091. https://doi.org/10.1371/journal.pone.0003091

APA

Kamei, H., Lu, L., Jiao, S., Li, Y., Nielsen, C. G., Laursen, L. S., Oxvig, C., Zhou, J., & Duan, C. (2008). Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish. P L o S One, 3(8), e3091. https://doi.org/10.1371/journal.pone.0003091

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MLA

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Author

Kamei, Hiroyasu ; Lu, Ling ; Jiao, Shuang ; Li, Yun ; Nielsen, Claus Gyrup ; Laursen, Lisbeth Schmidt ; Oxvig, Claus ; Zhou, Jianfeng ; Duan, Cunming. / Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish. In: P L o S One. 2008 ; Vol. 3, No. 8. pp. e3091.

Bibtex

@article{77302440780b11ddb7fc000ea68e967b,
title = "Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish",
abstract = "Background: Gene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish is uniquely positioned to provide insight into the process of functional gene evolution due to its amenability to genetic and experimental manipulation and because it possess a large number of duplicated genes.Methodology/Principal Findings: We report the identification and characterization of two hypoxia-inducible genes in zebrafish that are co-ortholgs of human IGF binding protein-1 (IGFBP-1). IGFBP-1 is a secreted protein that binds to IGF and modulates IGF actions in somatic growth, development, and aging. Like their human and mouse counterparts, in adultzebrafish igfbp-1a and igfbp-1b are exclusively expressed in the liver. During embryogenesis, the two genes are expressed in overlapping spatial domains but with distinct temporal patterns. While zebrafish IGFBP-1a mRNA was easily detected throughout embryogenesis, IGFBP-1b mRNA was detectable only in advanced stages. Hypoxia induces igfbp-1a expression in early embryogenesis, but induces the igfbp-1b expression later in embryogenesis. Both IGFBP-1a and -b are capable of IGF binding, but IGFBP-1b has much lower affinities for IGF-I and -II because of greater dissociation rates. Overexpression ofIGFBP-1a and -1b in zebrafish embryos caused significant decreases in growth and developmental rates. When tested in cultured zebrafish embryonic cells, IGFBP-1a and -1b both inhibited IGF-1-induced cell proliferation but the activity of IGFBP-1b was significantly weaker.Conclusions/Significance: These results indicate subfunction partitioning of the duplicated IGFBP-1 genes at the levels of gene expression, physiological regulation, protein structure, and biological actions. The duplicated IGFBP-1 may provide additional flexibility in fine-tuning IGF signaling activities under hypoxia and other catabolic conditions. ",
author = "Hiroyasu Kamei and Ling Lu and Shuang Jiao and Yun Li and Nielsen, {Claus Gyrup} and Laursen, {Lisbeth Schmidt} and Claus Oxvig and Jianfeng Zhou and Cunming Duan",
year = "2008",
month = dec,
doi = "10.1371/journal.pone.0003091",
language = "English",
volume = "3",
pages = "e3091",
journal = "P L o S One",
issn = "1932-6203",
publisher = "public library of science",
number = "8",

}

RIS

TY - JOUR

T1 - Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish

AU - Kamei, Hiroyasu

AU - Lu, Ling

AU - Jiao, Shuang

AU - Li, Yun

AU - Nielsen, Claus Gyrup

AU - Laursen, Lisbeth Schmidt

AU - Oxvig, Claus

AU - Zhou, Jianfeng

AU - Duan, Cunming

PY - 2008/12

Y1 - 2008/12

N2 - Background: Gene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish is uniquely positioned to provide insight into the process of functional gene evolution due to its amenability to genetic and experimental manipulation and because it possess a large number of duplicated genes.Methodology/Principal Findings: We report the identification and characterization of two hypoxia-inducible genes in zebrafish that are co-ortholgs of human IGF binding protein-1 (IGFBP-1). IGFBP-1 is a secreted protein that binds to IGF and modulates IGF actions in somatic growth, development, and aging. Like their human and mouse counterparts, in adultzebrafish igfbp-1a and igfbp-1b are exclusively expressed in the liver. During embryogenesis, the two genes are expressed in overlapping spatial domains but with distinct temporal patterns. While zebrafish IGFBP-1a mRNA was easily detected throughout embryogenesis, IGFBP-1b mRNA was detectable only in advanced stages. Hypoxia induces igfbp-1a expression in early embryogenesis, but induces the igfbp-1b expression later in embryogenesis. Both IGFBP-1a and -b are capable of IGF binding, but IGFBP-1b has much lower affinities for IGF-I and -II because of greater dissociation rates. Overexpression ofIGFBP-1a and -1b in zebrafish embryos caused significant decreases in growth and developmental rates. When tested in cultured zebrafish embryonic cells, IGFBP-1a and -1b both inhibited IGF-1-induced cell proliferation but the activity of IGFBP-1b was significantly weaker.Conclusions/Significance: These results indicate subfunction partitioning of the duplicated IGFBP-1 genes at the levels of gene expression, physiological regulation, protein structure, and biological actions. The duplicated IGFBP-1 may provide additional flexibility in fine-tuning IGF signaling activities under hypoxia and other catabolic conditions.

AB - Background: Gene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish is uniquely positioned to provide insight into the process of functional gene evolution due to its amenability to genetic and experimental manipulation and because it possess a large number of duplicated genes.Methodology/Principal Findings: We report the identification and characterization of two hypoxia-inducible genes in zebrafish that are co-ortholgs of human IGF binding protein-1 (IGFBP-1). IGFBP-1 is a secreted protein that binds to IGF and modulates IGF actions in somatic growth, development, and aging. Like their human and mouse counterparts, in adultzebrafish igfbp-1a and igfbp-1b are exclusively expressed in the liver. During embryogenesis, the two genes are expressed in overlapping spatial domains but with distinct temporal patterns. While zebrafish IGFBP-1a mRNA was easily detected throughout embryogenesis, IGFBP-1b mRNA was detectable only in advanced stages. Hypoxia induces igfbp-1a expression in early embryogenesis, but induces the igfbp-1b expression later in embryogenesis. Both IGFBP-1a and -b are capable of IGF binding, but IGFBP-1b has much lower affinities for IGF-I and -II because of greater dissociation rates. Overexpression ofIGFBP-1a and -1b in zebrafish embryos caused significant decreases in growth and developmental rates. When tested in cultured zebrafish embryonic cells, IGFBP-1a and -1b both inhibited IGF-1-induced cell proliferation but the activity of IGFBP-1b was significantly weaker.Conclusions/Significance: These results indicate subfunction partitioning of the duplicated IGFBP-1 genes at the levels of gene expression, physiological regulation, protein structure, and biological actions. The duplicated IGFBP-1 may provide additional flexibility in fine-tuning IGF signaling activities under hypoxia and other catabolic conditions.

U2 - 10.1371/journal.pone.0003091

DO - 10.1371/journal.pone.0003091

M3 - Journal article

C2 - 18769480

VL - 3

SP - e3091

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 8

ER -