Analysis of TPI gene promoter variation in three sub-Saharan Africa population samples
Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants ‐5A→G, ‐8G→A and ‐24T→G. Three haplotypes were identified in the three populations: the haplotype ‐5A‐8G‐24T (average frequency 65.3%) and two less common haplotypes ‐5G‐8G‐24T (averag...
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| Published in | American journal of human biology Vol. 21; no. 1; pp. 118 - 120 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.01.2009
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| Online Access | Get full text |
| ISSN | 1042-0533 1520-6300 1520-6300 |
| DOI | 10.1002/ajhb.20819 |
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| Abstract | Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants ‐5A→G, ‐8G→A and ‐24T→G. Three haplotypes were identified in the three populations: the haplotype ‐5A‐8G‐24T (average frequency 65.3%) and two less common haplotypes ‐5G‐8G‐24T (average frequency 24.7%) and ‐5G‐8A‐24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype ‐5A‐8G‐24T in 139 chromosomes and one subject heterozygous for haplotype ‐5G‐8A‐24G. The exact test of sample differentiation among three groups of malaria‐infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub‐Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem. Am. J. Hum. Biol., 2009. © 2008 Wiley‐Liss, Inc. |
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| AbstractList | Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants ‐5A→G, ‐8G→A and ‐24T→G. Three haplotypes were identified in the three populations: the haplotype ‐5A‐8G‐24T (average frequency 65.3%) and two less common haplotypes ‐5G‐8G‐24T (average frequency 24.7%) and ‐5G‐8A‐24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype ‐5A‐8G‐24T in 139 chromosomes and one subject heterozygous for haplotype ‐5G‐8A‐24G. The exact test of sample differentiation among three groups of malaria‐infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub‐Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem. Am. J. Hum. Biol., 2009. © 2008 Wiley‐Liss, Inc. Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants -5A-->G, -8G-->A and -24T-->G. Three haplotypes were identified in the three populations: the haplotype -5A-8G-24T (average frequency 65.3%) and two less common haplotypes -5G-8G-24T (average frequency 24.7%) and -5G-8A-24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype -5A-8G-24T in 139 chromosomes and one subject heterozygous for haplotype -5G-8A-24G. The exact test of sample differentiation among three groups of malaria-infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub-Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem.Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants -5A-->G, -8G-->A and -24T-->G. Three haplotypes were identified in the three populations: the haplotype -5A-8G-24T (average frequency 65.3%) and two less common haplotypes -5G-8G-24T (average frequency 24.7%) and -5G-8A-24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype -5A-8G-24T in 139 chromosomes and one subject heterozygous for haplotype -5G-8A-24G. The exact test of sample differentiation among three groups of malaria-infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub-Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem. Population samples from Angola, Mozambique, and S. Tome e Principe were screened for the TPI gene promoter variants -5AG, -8GA and -24TG. Three haplotypes were identified in the three populations: the haplotype -5A-8G-24T (average frequency 65.3%) and two less common haplotypes -5G-8G-24T (average frequency 24.7%) and -5G-8A-24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype -5A-8G-24T in 139 chromosomes and one subject heterozygous for haplotype -5G-8A-24G. The exact test of sample differentiation among three groups of malaria-infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub-Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem. Am. J. Hum. Biol., 2009. Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants -5A-->G, -8G-->A and -24T-->G. Three haplotypes were identified in the three populations: the haplotype -5A-8G-24T (average frequency 65.3%) and two less common haplotypes -5G-8G-24T (average frequency 24.7%) and -5G-8A-24T (average frequency 10.0%). A population sample from Central Portugal showed the haplotype -5A-8G-24T in 139 chromosomes and one subject heterozygous for haplotype -5G-8A-24G. The exact test of sample differentiation among three groups of malaria-infected individuals classified according to the severity of the disease showed no significant differences. We confirmed TPI gene diversity in sub-Saharan Africa, but we could not detect any association between TPI promoter variation and a malarial protective effect. Larger scale epidemiological studies are thus required to clarify this putative mechanism of natural host defense against this worldwide public health problem. |
| Author | Machado, Patrícia Lopes, Dinora Alonso, Pedro L. Amorim, António Nogueira, Fátima Varandas, Luís Manco, Licínio Do Rosário, Virgílio E. Arez, Ana Paula De Jesus Trovoada, Maria |
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| References | Marques PX,Saúte F,Pinto VV,Cardoso S,Pinto J,Alonso PL,do Rosário VE,Arez AP. 2005. Plasmodium species mixed infections in two ecologically different areas of Manhiça district, Mozambique. Int J Biol Sci 1: 96-102. Luzzatto L. 2006. Glucose 6-phosphate dehydrogenase deficiency: from genotype to phenotype. Haematologica 91: 1303-1306. Schneider AS. 2000. Triosephosphate isomerase deficiency: historical perspectives and molecular aspects. Baillieres Best Pract Res Clin Haematol 13: 119-140. Schneider A,Forman L,Westwood B,Yim C,Lin J,Singh S,Beutler E. 1998. The relationship of the -5, -8, and -24 variant alleles in African Americans to triosephosphate isomerase (TPI) enzyme activity and to TPI deficiency. Blood 92: 2959-2962. Humphries A,Ationu A,Lalloz MR,Layton DM. 1999a. Ancestral origin of variation in the triosephosphate isomerase gene promoter. Hum Genet 104: 486-491. Snounou G,Viriyakosol S,Zhu XP,Jarra W,Pinheiro L,do Rosário VE,Thaithong S,Brown KN. 1993. High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction. Mol Biochem Parasitol 1: 315-320. Excoffier L,Laval G,Schneider S. 2005. Arlequin (version 3.0): An integrated software package for population genetics data analysis. Evol Bioinformatics 1: 47-50. Fleming AF,Storey J,Molineaux L,Iroko EA,Attai EDE. 1979. Abnormal haemoglobins in the Sudan savanna of Nigeria, I: prevalence of haemoglobins and relationship between sickle cell trait, malaria, and survival. Ann Trop Med Parasitol 73: 161-172. Humphries A,Ationu A,Wild B,Layton DM. 1999b. The consequence of nucleotide substitutions in the triosephosphate isomerase (TPI) gene promoter. Blood Cells Mol Dis 25: 210-217. Raymond M,Rousset F. 1995. An exact test for population differentiation. Evolution 49: 1280-1283. WHO. 2000. Severe falciparum malaria. Trans R Soc Trop Med Hyg 94( Suppl 1): 1-90. 2000; 94 1999a; 104 1999b; 25 2006; 91 2005; 1 1998; 92 1995; 49 1993; 1 2000; 13 1979; 73 e_1_2_1_7_1 e_1_2_1_8_1 Schneider A (e_1_2_1_10_1) 1998; 92 e_1_2_1_5_1 e_1_2_1_3_1 e_1_2_1_12_1 e_1_2_1_4_1 e_1_2_1_2_1 e_1_2_1_11_1 Luzzatto L (e_1_2_1_6_1) 2006; 91 e_1_2_1_9_1 |
| References_xml | – reference: Schneider A,Forman L,Westwood B,Yim C,Lin J,Singh S,Beutler E. 1998. The relationship of the -5, -8, and -24 variant alleles in African Americans to triosephosphate isomerase (TPI) enzyme activity and to TPI deficiency. Blood 92: 2959-2962. – reference: Marques PX,Saúte F,Pinto VV,Cardoso S,Pinto J,Alonso PL,do Rosário VE,Arez AP. 2005. Plasmodium species mixed infections in two ecologically different areas of Manhiça district, Mozambique. Int J Biol Sci 1: 96-102. – reference: WHO. 2000. Severe falciparum malaria. Trans R Soc Trop Med Hyg 94( Suppl 1): 1-90. – reference: Humphries A,Ationu A,Lalloz MR,Layton DM. 1999a. Ancestral origin of variation in the triosephosphate isomerase gene promoter. Hum Genet 104: 486-491. – reference: Humphries A,Ationu A,Wild B,Layton DM. 1999b. The consequence of nucleotide substitutions in the triosephosphate isomerase (TPI) gene promoter. Blood Cells Mol Dis 25: 210-217. – reference: Raymond M,Rousset F. 1995. An exact test for population differentiation. Evolution 49: 1280-1283. – reference: Snounou G,Viriyakosol S,Zhu XP,Jarra W,Pinheiro L,do Rosário VE,Thaithong S,Brown KN. 1993. High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction. Mol Biochem Parasitol 1: 315-320. – reference: Schneider AS. 2000. Triosephosphate isomerase deficiency: historical perspectives and molecular aspects. Baillieres Best Pract Res Clin Haematol 13: 119-140. – reference: Excoffier L,Laval G,Schneider S. 2005. Arlequin (version 3.0): An integrated software package for population genetics data analysis. Evol Bioinformatics 1: 47-50. – reference: Luzzatto L. 2006. Glucose 6-phosphate dehydrogenase deficiency: from genotype to phenotype. Haematologica 91: 1303-1306. – reference: Fleming AF,Storey J,Molineaux L,Iroko EA,Attai EDE. 1979. Abnormal haemoglobins in the Sudan savanna of Nigeria, I: prevalence of haemoglobins and relationship between sickle cell trait, malaria, and survival. Ann Trop Med Parasitol 73: 161-172. – volume: 1 start-page: 315 year: 1993 end-page: 320 article-title: High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction publication-title: Mol Biochem Parasitol – volume: 49 start-page: 1280 year: 1995 end-page: 1283 article-title: An exact test for population differentiation publication-title: Evolution – volume: 91 start-page: 1303 year: 2006 end-page: 1306 article-title: Glucose 6‐phosphate dehydrogenase deficiency: from genotype to phenotype publication-title: Haematologica – volume: 13 start-page: 119 year: 2000 end-page: 140 article-title: Triosephosphate isomerase deficiency: historical perspectives and molecular aspects publication-title: Baillieres Best Pract Res Clin Haematol – volume: 104 start-page: 486 year: 1999a end-page: 491 article-title: Ancestral origin of variation in the triosephosphate isomerase gene promoter publication-title: Hum Genet – volume: 92 start-page: 2959 year: 1998 end-page: 2962 article-title: The relationship of the ‐5, ‐8, and ‐24 variant alleles in African Americans to triosephosphate isomerase (TPI) enzyme activity and to TPI deficiency publication-title: Blood – volume: 1 start-page: 47 year: 2005 end-page: 50 article-title: Arlequin (version 3.0): An integrated software package for population genetics data analysis publication-title: Evol Bioinformatics – volume: 1 start-page: 96 year: 2005 end-page: 102 article-title: species mixed infections in two ecologically different areas of Manhiça district, Mozambique publication-title: Int J Biol Sci – volume: 94 start-page: 1 issue: Suppl 1 year: 2000 end-page: 90 article-title: Severe malaria publication-title: Trans R Soc Trop Med Hyg – volume: 73 start-page: 161 year: 1979 end-page: 172 article-title: Abnormal haemoglobins in the Sudan savanna of Nigeria, I: prevalence of haemoglobins and relationship between sickle cell trait, malaria, and survival publication-title: Ann Trop Med Parasitol – volume: 25 start-page: 210 year: 1999b end-page: 217 article-title: The consequence of nucleotide substitutions in the triosephosphate isomerase (TPI) gene promoter publication-title: Blood Cells Mol Dis – ident: e_1_2_1_2_1 doi: 10.1111/j.1365-294X.2006.03067.x – ident: e_1_2_1_9_1 doi: 10.1053/beha.2000.0061 – ident: e_1_2_1_11_1 doi: 10.1016/0166-6851(93)90077-B – ident: e_1_2_1_3_1 doi: 10.1080/00034983.1979.11687243 – ident: e_1_2_1_7_1 doi: 10.7150/ijbs.1.96 – volume: 92 start-page: 2959 year: 1998 ident: e_1_2_1_10_1 article-title: The relationship of the ‐5, ‐8, and ‐24 variant alleles in African Americans to triosephosphate isomerase (TPI) enzyme activity and to TPI deficiency publication-title: Blood doi: 10.1182/blood.V92.8.2959 – ident: e_1_2_1_4_1 doi: 10.1007/s004390050992 – ident: e_1_2_1_5_1 doi: 10.1006/bcmd.1999.0246 – ident: e_1_2_1_8_1 doi: 10.1111/j.1558-5646.1995.tb04456.x – ident: e_1_2_1_12_1 doi: 10.1016/S0035-9203(00)90300-6 – volume: 91 start-page: 1303 year: 2006 ident: e_1_2_1_6_1 article-title: Glucose 6‐phosphate dehydrogenase deficiency: from genotype to phenotype publication-title: Haematologica |
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| Snippet | Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants ‐5A→G, ‐8G→A and ‐24T→G. Three haplotypes... Population samples from Angola, Mozambique, and S. Tomé e Príncipe were screened for the TPI gene promoter variants -5A-->G, -8G-->A and -24T-->G. Three... Population samples from Angola, Mozambique, and S. Tome e Principe were screened for the TPI gene promoter variants -5AG, -8GA and -24TG. Three haplotypes were... |
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| SubjectTerms | Africa South of the Sahara Female Genetic Variation Haplotypes Humans Malaria - genetics Male Population Groups - genetics Portugal Promoter Regions, Genetic - genetics Triose-Phosphate Isomerase - genetics |
| Title | Analysis of TPI gene promoter variation in three sub-Saharan Africa population samples |
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