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2. Structural diversity and African origin of the 17q21.31 inversion polymorphism

Author

Steinberg, Karyn Meltz, Antonacci, Francesca, Sudmant, Peter H, Kidd, Jeffrey M, Campbell, Catarina D, Vives, Laura, Malig, Maika, Scheinfeldt, Laura, Beggs, William, Ibrahim, Muntaser, Lema, Godfrey, Nyambo, Thomas B, Omar, Sabah A, Bodo, Jean-Marie, Froment, Alain, Donnelly, Michael P, Kidd, Kenneth K, Tishkoff, Sarah A, and Eichler, Evan E

Subjects
Genetics, Africa, Black People, Chromosome Inversion, Chromosomes, Human, Pair 17, Evolution, Molecular, Gene Frequency, Haplotypes, Humans, In Situ Hybridization, Fluorescence, Linkage Disequilibrium, Phylogeny, Polymorphism, Genetic, Polymorphism, Single Nucleotide, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

The 17q21.31 inversion polymorphism exists either as direct (H1) or inverted (H2) haplotypes with differential predispositions to disease and selection. We investigated its genetic diversity in 2,700 individuals, with an emphasis on African populations. We characterize eight structural haplotypes due to complex rearrangements that vary in size from 1.08-1.49 Mb and provide evidence for a 30-kb H1-H2 double recombination event. We show that recurrent partial duplications of the KANSL1 gene have occurred on both the H1 and H2 haplotypes and have risen to high frequency in European populations. We identify a likely ancestral H2 haplotype (H2') lacking these duplications that is enriched among African hunter-gatherer groups yet essentially absent from West African populations. Whereas H1 and H2 segmental duplications arose independently and before human migration out of Africa, they have reached high frequencies recently among Europeans, either because of extraordinary genetic drift or selective sweeps.

Published
2012

3. A Locus at 5q33.3 Confers Resistance to Tuberculosis in Highly Susceptible Individuals

Author

Sobota, Rafal S., Stein, Catherine M., Kodaman, Nuri, Scheinfeldt, Laura B., Maro, Isaac, Wieland-Alter, Wendy, Igo, Robert P., Jr., Magohe, Albert, Malone, LaShaunda L., Chervenak, Keith, Hall, Noemi B., Modongo, Chawangwa, Zetola, Nicola, Matee, Mecky, Joloba, Moses, Froment, Alain, Nyambo, Thomas B., Moore, Jason H., Scott, William K., Lahey, Timothy, Boom, W. Henry, von Reyn, C. Fordham, Tishkoff, Sarah A., Sirugo, Giorgio, and Williams, Scott M.

Published
2016
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4. Additional file 1 of The genetic and evolutionary basis of gene expression variation in East Africans

Author

Kelly, Derek E., Ramdas, Shweta, Ma, Rong, Rawlings-Goss, Renata A., Grant, Gregory R., Ranciaro, Alessia, Hirbo, Jibril B., Beggs, William, Yeager, Meredith, Chanock, Stephen, Nyambo, Thomas B., Omar, Sabah A., Woldemeskel, Dawit, Belay, Gurja, Li, Hongzhe, Brown, Christopher D., and Tishkoff, Sarah A.

Abstract

Additional file 1: Fig S1. Principal Component Analysis of East African and 1000 Genome Project. Fig S2. ADMIXTURE analysis across K values 2-12. Fig S3. Genomic context of tQTLs. Fig S4. π1 of eQTL p-values of SNP-gene pairs ascertained as sQTLs. Fig S5. π1 between sQTLs and eQTLs across gene length deciles. Fig S6. π1 value of ascertained eQTLs and sQTLs in GTEx. Fig S7. Mapping statistics from STAR. Fig S8. Frequency and LD differences between African samples and 1000 Genomes EURpopulations. Fig S9. tQTL effect size vs MAF. Fig S10. Fraction of FST outliers among eQTLs and sQTLs compared with matched background. Fig S11. Population-specific FST outliers. Fig. S12. Global frequencies of SNPs associated with pigmentation variation and TMEM216 expression and splicing. Fig S13. Colocalization of Mursi PBS and d-statistics with TMEM216 eQTLs. Fig S14. Colocalization of Mursi PBS and d-statistics with pigmentation GWAS. Fig S15. eQTL associations for TMEM216 across populations. Fig S16. ‘LocusCompare’ plots of African pigmentation GWAS and GTEx v8 eQTLs. Fig S17. ‘LocusCompare’ plots of African pigmentation GWAS and GTEx v8 sQTLs.

Published
2023
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5. Additional file 3 of The genetic and evolutionary basis of gene expression variation in East Africans

Author

Kelly, Derek E., Ramdas, Shweta, Ma, Rong, Rawlings-Goss, Renata A., Grant, Gregory R., Ranciaro, Alessia, Hirbo, Jibril B., Beggs, William, Yeager, Meredith, Chanock, Stephen, Nyambo, Thomas B., Omar, Sabah A., Woldemeskel, Dawit, Belay, Gurja, Li, Hongzhe, Brown, Christopher D., and Tishkoff, Sarah A.

Abstract

Additional file 3. Reviewhistory.

Published
2023
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8. The Genetic Structure and History of Africans and African Americans

Author

Tishkoff, Sarah A., Reed, Floyd A., Friedlaender, Françoise R., Ehret, Christopher, Ranciaro, Alessia, Froment, Alain, Hirbo, Jibril B., Awomoyi, Agnes A., Bodo, Jean-Marie, Doumbo, Ogobara, Ibrahim, Muntaser, Juma, Abdalla T., Kotze, Maritha J., Lema, Godfrey, Moore, Jason H., Mortensen, Holly, Nyambo, Thomas B., Omar, Sabah A., Powell, Kweli, Pretorius, Gideon S., Smith, Michael W., Thera, Mahamadou A., Wambebe, Charles, Weber, James L., and Williams, Scott M.

Published
2009
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10. 1284-P: Genetic and Lifestyle Associations with Cardiometabolic Traits and Diabetes Risk Factors in Ethnically Diverse Africans

Author

HUI, DANIEL, primary, HARRIS, DANIEL, additional, MCQUILLAN, MICHAEL, additional, HANSEN, MATTHEW, additional, RANCIARO, ALESSIA, additional, BEGGS, WILLIAM, additional, MPOLOKA, SUNUNGUKO W., additional, WOLDEMESKEL, DAWIT, additional, NJAMNSHI, ALFRED K.K., additional, NYAMBO, THOMAS B., additional, CHANOCK, STEPHEN, additional, and TISHKOFF, SARAH A., additional

Published
2022
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12. 191-LB: Impact of Subsistence and Genetics on Lipid Profiles in Ethnically Diverse Africans

Author

MA, RONG, primary, HANSEN, MATTHEW, additional, RANCIARO, ALESSIA, additional, THOMPSON, SIMON R., additional, BEGGS, WILLIAM, additional, MPOLOKA, SUNUNGUKO W., additional, MOKONE, GAONYADIWE G., additional, NYAMBO, THOMAS B., additional, MICHAILIDIS, GEORGE, additional, LI, HONGZHE, additional, BURANT, CHARLES, additional, and TISHKOFF, SARAH A., additional

Published
2021
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13. Genetics and geography of leukocyte telomere length in sub-Saharan Africans

Author

Hunt, Steven C, primary, Hansen, Matthew E B, additional, Verhulst, Simon, additional, McQuillan, Michael A, additional, Beggs, William, additional, Lai, Tsung-Po, additional, Mokone, Gaonyadiwe G, additional, Mpoloka, Sununguko Wata, additional, Meskel, Dawit Wolde, additional, Belay, Gurja, additional, Nyambo, Thomas B, additional, Abnet, Christian C, additional, Yeager, Meredith, additional, Chanock, Stephen J, additional, Province, Michael A, additional, Williams, Scott M, additional, Aviv, Abraham, additional, and Tishkoff, Sarah A, additional

Published
2020
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17. Drug resistance to sulphadoxine-pyrimethamine in Plasmodium falciparum malaria in Mlimba, Tanzania

Author

Balthazary Sakurani T, Malisa Allen L, Mutayoba Benezeth M, Mbugi Erasto V, Nyambo Thomas B, and Mshinda Hassan

Subjects
Arctic medicine. Tropical medicine, RC955-962, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Sulphadoxine-pyrimethamine (SP) has been and is currently used for treatment of uncomplicated Plasmodium falciparum malaria in many African countries. Nevertheless, the response of parasites to SP treatment has shown significant variation between individuals. Methods The genes for dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) were used as markers, to investigate parasite resistance to SP in 141 children aged less than 5 years. Parasite DNA was extracted by Chelex method from blood samples collected and preserved on filter papers. Subsequently, polymerase chain reaction (PCR) and restriction fragment length polymorphism (PCR-RFLP) were applied to detect the SP resistance-associated point mutations on dhfr and dhps. Commonly reported point mutations at codons 51, 59, 108 and 164 in the dhfr and codons 437, 540 and 581 in the dhps domains were examined. Results Children infected with parasites harbouring a range of single to quintuple dhfr/dhps mutations were erratically cured with SP. However, the quintuple dhfr/dhps mutant genotypes were mostly associated with treatment failures. High proportion of SP resistance-associated point mutations was detected in this study but the adequate clinical response (89.4%) observed clinically at day 14 of follow up reflects the role of semi-immunity protection and parasite clearance in the population. Conclusion In monitoring drug resistance to SP, concurrent studies on possible confounding factors pertaining to development of resistance in falciparum malaria should be considered. The SP resistance potential detected in this study, cautions on its useful therapeutic life as an interim first-line drug against malaria in Tanzania and other malaria-endemic countries.

Published
2006
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18. タンザニアの免疫血清による熱帯熱マラリア原虫の試験管内増殖阻害

Author

Nyambo, Thomas B. and Kanbara, Hiroji

Subjects
parasitic diseases
Abstract

The inhibition titers of sera from adult residents in Dar es Salaam, Tanzania to intraerythrocytic growth of Plasmodium falciparum were not correlated to their antibody titers by immunofluorescence and enzyme immunoassay, and did not exhibit specificity to the strain with a certain MSA-1 gene. Another inhibitory factor (s) was found in a low molecular fraction with molecular weight less than 30,000 that was separated from a high molecular fraction by centrifugation on a meriibrane filter (centriprep-30, Amicon). This factor induced morphological changes of intraerythrocytic parasites and was thought to correspond to crisis form factor (CFF) by Jensen et al.(1982). The factor was shown to remain in the serum of an adult Tanzanian who had lived in a non-malarious area six months prior to the commencement of this study and to be contained in a hyperimmune serum from a Japanese patient even though on a low level, 日本熱帯医学会雑誌, vol.22(4), pp.211-215; 1994

Published
1994

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