Study of four genes belonging to the folate pathway: transcobalamin 2 is involved in the onset of non-syndromic cleft lip with or without cleft palate
Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So...
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Published in | Human mutation Vol. 27; no. 3; p. 294 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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01.03.2006
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Abstract | Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So far, only the MTHFR gene has been extensively investigated as a risk factor for CL/P, while little has been done to test genetic variations in the folate biosynthetic pathways that may influence the infant's susceptibility to these birth defects. To date, this paper presents the first attempt to verify the involvement of four genes belonging to the folate pathway in nonsyndromic cleft onset. We used a case‐parent triad design to test for linkage disequilibrium in the case of seven SNPs mapping on four different genes: transcobalamin 1 and 2 (TCN1 and TCN2), methionine synthase (MTR), and MTR reductase (MTRR). Our finding suggests that TCN2 is involved in causing CL/P. Indeed, significant overtransmission of the C allele was observed at the polymorphism c.776C>G (p.Pro259Arg) to the affected offspring (P=0.01). Results obtained with additional TCN2 polymorphisms suggest that c.776C>G may be functionally related to CL/P. However, because conflicting data exist with regard to the effect of the polymorphism in transcobalamin 2 function or in perturbing plasma levels of key molecules in the folate pathway, further investigation is warranted to confirm our data. © 2006 Wiley‐Liss, Inc. |
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AbstractList | Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So far, only the MTHFR gene has been extensively investigated as a risk factor for CL/P, while little has been done to test genetic variations in the folate biosynthetic pathways that may influence the infant's susceptibility to these birth defects. To date, this paper presents the first attempt to verify the involvement of four genes belonging to the folate pathway in nonsyndromic cleft onset. We used a case-parent triad design to test for linkage disequilibrium in the case of seven SNPs mapping on four different genes: transcobalamin 1 and 2 (TCN1 and TCN2), methionine synthase (MTR), and MTR reductase (MTRR). Our finding suggests that TCN2 is involved in causing CL/P. Indeed, significant overtransmission of the C allele was observed at the polymorphism c.776C>G (p.Pro259Arg) to the affected offspring (P=0.01). Results obtained with additional TCN2 polymorphisms suggest that c.776C>G may be functionally related to CL/P. However, because conflicting data exist with regard to the effect of the polymorphism in transcobalamin 2 function or in perturbing plasma levels of key molecules in the folate pathway, further investigation is warranted to confirm our data. © 2006 Wiley-Liss, Inc. Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So far, only the MTHFR gene has been extensively investigated as a risk factor for CL/P, while little has been done to test genetic variations in the folate biosynthetic pathways that may influence the infant's susceptibility to these birth defects. To date, this paper presents the first attempt to verify the involvement of four genes belonging to the folate pathway in nonsyndromic cleft onset. We used a case-parent triad design to test for linkage disequilibrium in the case of seven SNPs mapping on four different genes: transcobalamin 1 and 2 (TCN1 and TCN2), methionine synthase (MTR), and MTR reductase (MTRR). Our finding suggests that TCN2 is involved in causing CL/P. Indeed, significant overtransmission of the C allele was observed at the polymorphism c.776C>G (p.Pro259Arg) to the affected offspring (P=0.01). Results obtained with additional TCN2 polymorphisms suggest that c.776C>G may be functionally related to CL/P. However, because conflicting data exist with regard to the effect of the polymorphism in transcobalamin 2 function or in perturbing plasma levels of key molecules in the folate pathway, further investigation is warranted to confirm our data. Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So far, only the MTHFR gene has been extensively investigated as a risk factor for CL/P, while little has been done to test genetic variations in the folate biosynthetic pathways that may influence the infant's susceptibility to these birth defects. To date, this paper presents the first attempt to verify the involvement of four genes belonging to the folate pathway in nonsyndromic cleft onset. We used a case-parent triad design to test for linkage disequilibrium in the case of seven SNPs mapping on four different genes: transcobalamin 1 and 2 (TCN1 and TCN2), methionine synthase (MTR), and MTR reductase (MTRR). Our finding suggests that TCN2 is involved in causing CL/P. Indeed, significant overtransmission of the C allele was observed at the polymorphism c.776C>G (p.Pro259Arg) to the affected offspring (P=0.01). Results obtained with additional TCN2 polymorphisms suggest that c.776C>G may be functionally related to CL/P. However, because conflicting data exist with regard to the effect of the polymorphism in transcobalamin 2 function or in perturbing plasma levels of key molecules in the folate pathway, further investigation is warranted to confirm our data. |
Author | Carinci, Francesco Giovanni Morselli, Paolo Carinci, Paolo Scapoli, Luca Palmieri, Annalisa Pezzetti, Furio Martinelli, Marcella Baciliero, Ugo Padula, Ernesto |
Author_xml | – sequence: 1 givenname: Marcella surname: Martinelli fullname: Martinelli, Marcella organization: Department of Morphology and Embryology, Section of Histology and Embryology, University of Ferrara, Ferrara, Italy – sequence: 2 givenname: Luca surname: Scapoli fullname: Scapoli, Luca email: luca.scapoli2@unibo.it organization: Department of Histology, Embryology and Applied Biology; Centre of Molecular Genetics, CARISBO Foundation, University of Bologna, Bologna, Italy – sequence: 3 givenname: Annalisa surname: Palmieri fullname: Palmieri, Annalisa organization: Department of Histology, Embryology and Applied Biology; Centre of Molecular Genetics, CARISBO Foundation, University of Bologna, Bologna, Italy – sequence: 4 givenname: Furio surname: Pezzetti fullname: Pezzetti, Furio organization: Department of Histology, Embryology and Applied Biology; Centre of Molecular Genetics, CARISBO Foundation, University of Bologna, Bologna, Italy – sequence: 5 givenname: Ugo surname: Baciliero fullname: Baciliero, Ugo organization: Department of Maxillo-Facial Surgery, San Bortolo Hospital, Vicenza, Italy – sequence: 6 givenname: Ernesto surname: Padula fullname: Padula, Ernesto organization: Department of Maxillo-Facial Surgery, San Bortolo Hospital, Vicenza, Italy – sequence: 7 givenname: Paolo surname: Carinci fullname: Carinci, Paolo organization: Department of Histology, Embryology and Applied Biology; Centre of Molecular Genetics, CARISBO Foundation, University of Bologna, Bologna, Italy – sequence: 8 givenname: Paolo surname: Giovanni Morselli fullname: Giovanni Morselli, Paolo organization: Department of Surgical and Anesthesiologic Sciences, Sant'Orsola Hospital, Bologna, Italy – sequence: 9 givenname: Francesco surname: Carinci fullname: Carinci, Francesco organization: Department of Maxillo-Facial Surgery, University of Ferrara, Ferrara, Italy |
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SubjectTerms | 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase - genetics Alleles Cleft Lip - genetics cleft lip with or without cleft palate Cleft Palate - genetics Ferredoxin-NADP Reductase - genetics Folic Acid - metabolism Gene Expression Regulation Genetic Markers Genetic Predisposition to Disease Humans MTR MTRR orofacial cleft Polymorphism, Genetic Polymorphism, Single Nucleotide TCN1 TCN2 Transcobalamins - genetics |
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Title | Study of four genes belonging to the folate pathway: transcobalamin 2 is involved in the onset of non-syndromic cleft lip with or without cleft palate |
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