Common variants in signaling transcription-factor-binding sites drive phenotypic variability in red blood cell traits.

Common variants in signaling transcription-factor-binding sites drive phenotypic variability in red blood cell traits.
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DOI:
10.1038/s41588-020-00738-2
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发表时间:
2020-12
期刊:
影响因子:
30.8
通讯作者:
Zon LI
Zon LI
中科院分区:
生物学1区
文献类型:
--
作者:
Choudhuri A;Trompouki E;Abraham BJ;Colli LM;Kock KH;Mallard W;Yang ML;Vinjamur DS;Ghamari A;Sporrij A;Hoi K;Hummel B;Boatman S;Chan V;Tseng S;Nandakumar SK;Yang S;Lichtig A;Superdock M;Grimes SN;Bowman TV;Zhou Y;Takahashi S;Joehanes R;Cantor AB;Bauer DE;Ganesh SK;Rinn J;Albert PS;Bulyk ML;Chanock SJ;Young RA;Zon LI

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Genome-wide association studies (GWAS) identify genomic variants associated with human traits and diseases. Most trait-associated variants are located within cell type-specific enhancers, but the molecular mechanisms governing phenotypic variation are less understood. Here, we show that many enhancer-variants associated with red blood cell (RBC) traits map to enhancers that are co-bound by lineage-specific master transcription factors (MTFs) and signaling transcription factors (STFs) responsive to extracellular signals. The majority of enhancer variants resides on STF and not MTF motifs, perturbing DNA-binding by various STFs (BMP/TGFβ-directed SMADs or WNT-induced TCFs) and affecting target gene expression. Engineered human blood cells and expression quantitative trait loci (eQTL) analyses verify that disrupted STF binding leads to altered gene expression. Our results propose that the majority of the RBC trait-associated variants that reside on TF binding sequences falls in STF target sequences, suggesting that the phenotypic variation of RBC traits could stem from altered responsiveness to extracellular stimuli.
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