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Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells

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Published on: December 27, 2017

Platelet function is modified by common sequence variation in megakaryocyte super enhancers.

Romina Petersen^1,2, John J Lambourne^1,2, Biola M Javierre³

¹Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge CB2 0PT, UK.

Nature Communications

|July 14, 2017

Summary

Researchers linked genetic variants to platelet traits using epigenomic data. They found that variants in super enhancers significantly control platelet functions, advancing precision medicine.

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Area of Science:

Genomics
Molecular Biology
Precision Medicine

Background:

Genome-Wide Association Studies (GWAS) identify genetic variants linked to diseases.
Non-coding variants are challenging to link to specific genes and functions.
Understanding these links is crucial for precision medicine.

Purpose of the Study:

To determine the mechanisms connecting genetic variants to platelet quantitative traits.
To identify target genes for non-coding variants associated with platelet traits.

Main Methods:

Utilized cell type-matched epigenomic data.
Analyzed promoter long-range interactions.
Performed ex vivo validation and genome editing.

Main Results:

Identified potential regulatory functions for 75% (423 of 565) of non-coding variants associated with platelet traits.
Demonstrated that variants in super enhancers control archetypical platelet functions.

Conclusions:

Non-coding variants associated with platelet traits can be linked to target genes.
Super enhancers play a critical role in regulating platelet function, offering potential therapeutic targets.