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Coordinated gene expression during gilthead sea bream skeletogenesis and its disruption by nutritional hypervitaminosis A.

Fernández I, Darias M, Andree KB, Mazurais D, Zambonino-Infante JL, Gisbert E - BMC Dev. Biol. (2011)

Bottom Line: Present data reflects the specific gene expression patterns of several genes involved in larval fish RA signalling and skeletogenesis; and how specific gene disruption induced by a nutritional VA imbalance underlie the skeletal deformities.Our results are of basic interest for fish VA signalling and point out some of the potential molecular players involved in fish skeletogenesis.Increased incidences of skeletal deformities in gilthead sea bream fed with hypervitaminosis A were the likely ultimate consequence of specific gene expression disruption at critical development stages.

View Article: PubMed Central - HTML - PubMed

Affiliation: Unitat de Cultius Experimentals, IRTA Centre de Sant Carles de la Ràpita (IRTA-SCR), Crta, del Poble Nou s/n, 43540 - Sant Carles de la Ràpita (Spain) ignacio.fernandez@irta.es

ABSTRACT

Background: Vitamin A (VA) has a key role in vertebrate morphogenesis, determining body patterning and growth through the control of cell proliferation and differentiation processes. VA regulates primary molecular pathways of those processes by the binding of its active metabolite (retinoic acid) to two types of specific nuclear receptors: retinoic acid receptors (RARs) and retinoid X receptors (RXRs), which promote transcription of downstream target genes. This process is well known in most of higher vertebrates; however, scarce information is available regarding fishes. Therefore, in order to gain further knowledge of fish larval development and its disruption by nutritional VA imbalance, the relative expression of some RARs and RXRs, as well as several genes involved in morpho- and skeletogenesis such as peroxisome proliferator-activated receptors (PPARA, PPARB and PPARG); retinol-binding protein (RBP); insulin-like growth factors I and II (IGF1 and IGF2, respectively); bone morphogenetic protein 2 (Bmp2); transforming growth factor β-1 (TGFB1); and genes encoding different extracellular matrix (ECM) proteins such as matrix Gla protein (mgp), osteocalcin (bglap), osteopontin (SPP1), secreted protein acidic and rich in cysteine (SPARC) and type I collagen α1 chain (COL1A1) have been studied in gilthead sea bream.

Results: During gilthead sea bream larval development, specific expression profiles for each gene were tightly regulated during fish morphogenesis and correlated with specific morphogenetic events and tissue development. Dietary hypervitaminosis A during early larval development disrupted the normal gene expression profile for genes involved in RA signalling (RARA), VA homeostasis (RBP) and several genes encoding ECM proteins that are linked to skeletogenesis, such as bglap and mgp.

Conclusions: Present data reflects the specific gene expression patterns of several genes involved in larval fish RA signalling and skeletogenesis; and how specific gene disruption induced by a nutritional VA imbalance underlie the skeletal deformities. Our results are of basic interest for fish VA signalling and point out some of the potential molecular players involved in fish skeletogenesis. Increased incidences of skeletal deformities in gilthead sea bream fed with hypervitaminosis A were the likely ultimate consequence of specific gene expression disruption at critical development stages.

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Ontogenetic gene expression patterns of RBP (a), PPARA (b), PPARB (c), PPARG (d), IGF1 (e), IGF2 (f), Bmp2 (g), and TGFB1 (h). Gene expression measured as the mean expression ratio of the target gene with respect to the house-keeping gene (EF1α) at each sample time compared with initial sample time (2 dph). Different letters denote significant differences of the global gene expression (ANOVA, P < 0.05; n = 3).
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Figure 5: Ontogenetic gene expression patterns of RBP (a), PPARA (b), PPARB (c), PPARG (d), IGF1 (e), IGF2 (f), Bmp2 (g), and TGFB1 (h). Gene expression measured as the mean expression ratio of the target gene with respect to the house-keeping gene (EF1α) at each sample time compared with initial sample time (2 dph). Different letters denote significant differences of the global gene expression (ANOVA, P < 0.05; n = 3).

Mentions: There were no significant differences in the RBP gene expression profile during the larval development (ANOVA, P > 0.05; Figure 5a). PPARA expression was constant from 2 to 37 dph, whereas at 45 dph a peak of gene expression was noted (2.94 fold increase with respect to 2 dph larvae; P < 0.05; Figure 5b). PPARB expression remained constant from 2 to 60 dph (ANOVA, P > 0.05; Figure 5c). The PPARG expression level did not change from 2 to 52 dph; however, at the end of the study (60 dph), expression values were significantly higher than those mostly observed between 7 and 37 dph (ANOVA, P < 0.05; Figure 5d), but not significantly different to those observed at 2 dph.


Coordinated gene expression during gilthead sea bream skeletogenesis and its disruption by nutritional hypervitaminosis A.

Fernández I, Darias M, Andree KB, Mazurais D, Zambonino-Infante JL, Gisbert E - BMC Dev. Biol. (2011)

Ontogenetic gene expression patterns of RBP (a), PPARA (b), PPARB (c), PPARG (d), IGF1 (e), IGF2 (f), Bmp2 (g), and TGFB1 (h). Gene expression measured as the mean expression ratio of the target gene with respect to the house-keeping gene (EF1α) at each sample time compared with initial sample time (2 dph). Different letters denote significant differences of the global gene expression (ANOVA, P < 0.05; n = 3).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3045981&req=5

Figure 5: Ontogenetic gene expression patterns of RBP (a), PPARA (b), PPARB (c), PPARG (d), IGF1 (e), IGF2 (f), Bmp2 (g), and TGFB1 (h). Gene expression measured as the mean expression ratio of the target gene with respect to the house-keeping gene (EF1α) at each sample time compared with initial sample time (2 dph). Different letters denote significant differences of the global gene expression (ANOVA, P < 0.05; n = 3).
Mentions: There were no significant differences in the RBP gene expression profile during the larval development (ANOVA, P > 0.05; Figure 5a). PPARA expression was constant from 2 to 37 dph, whereas at 45 dph a peak of gene expression was noted (2.94 fold increase with respect to 2 dph larvae; P < 0.05; Figure 5b). PPARB expression remained constant from 2 to 60 dph (ANOVA, P > 0.05; Figure 5c). The PPARG expression level did not change from 2 to 52 dph; however, at the end of the study (60 dph), expression values were significantly higher than those mostly observed between 7 and 37 dph (ANOVA, P < 0.05; Figure 5d), but not significantly different to those observed at 2 dph.

Bottom Line: Present data reflects the specific gene expression patterns of several genes involved in larval fish RA signalling and skeletogenesis; and how specific gene disruption induced by a nutritional VA imbalance underlie the skeletal deformities.Our results are of basic interest for fish VA signalling and point out some of the potential molecular players involved in fish skeletogenesis.Increased incidences of skeletal deformities in gilthead sea bream fed with hypervitaminosis A were the likely ultimate consequence of specific gene expression disruption at critical development stages.

View Article: PubMed Central - HTML - PubMed

Affiliation: Unitat de Cultius Experimentals, IRTA Centre de Sant Carles de la Ràpita (IRTA-SCR), Crta, del Poble Nou s/n, 43540 - Sant Carles de la Ràpita (Spain) ignacio.fernandez@irta.es

ABSTRACT

Background: Vitamin A (VA) has a key role in vertebrate morphogenesis, determining body patterning and growth through the control of cell proliferation and differentiation processes. VA regulates primary molecular pathways of those processes by the binding of its active metabolite (retinoic acid) to two types of specific nuclear receptors: retinoic acid receptors (RARs) and retinoid X receptors (RXRs), which promote transcription of downstream target genes. This process is well known in most of higher vertebrates; however, scarce information is available regarding fishes. Therefore, in order to gain further knowledge of fish larval development and its disruption by nutritional VA imbalance, the relative expression of some RARs and RXRs, as well as several genes involved in morpho- and skeletogenesis such as peroxisome proliferator-activated receptors (PPARA, PPARB and PPARG); retinol-binding protein (RBP); insulin-like growth factors I and II (IGF1 and IGF2, respectively); bone morphogenetic protein 2 (Bmp2); transforming growth factor β-1 (TGFB1); and genes encoding different extracellular matrix (ECM) proteins such as matrix Gla protein (mgp), osteocalcin (bglap), osteopontin (SPP1), secreted protein acidic and rich in cysteine (SPARC) and type I collagen α1 chain (COL1A1) have been studied in gilthead sea bream.

Results: During gilthead sea bream larval development, specific expression profiles for each gene were tightly regulated during fish morphogenesis and correlated with specific morphogenetic events and tissue development. Dietary hypervitaminosis A during early larval development disrupted the normal gene expression profile for genes involved in RA signalling (RARA), VA homeostasis (RBP) and several genes encoding ECM proteins that are linked to skeletogenesis, such as bglap and mgp.

Conclusions: Present data reflects the specific gene expression patterns of several genes involved in larval fish RA signalling and skeletogenesis; and how specific gene disruption induced by a nutritional VA imbalance underlie the skeletal deformities. Our results are of basic interest for fish VA signalling and point out some of the potential molecular players involved in fish skeletogenesis. Increased incidences of skeletal deformities in gilthead sea bream fed with hypervitaminosis A were the likely ultimate consequence of specific gene expression disruption at critical development stages.

Show MeSH
Related in: MedlinePlus