Clonal expansion of DNMT3A-mutant hematopoietic stem cells is a risk factor for myeloid malignancies and other morbidities. A new study uses multi-modal single-cell genomics to characterize the myeloid differentiation bias of DNMT3A-mutated clones, and finds preferential hypomethylation of binding motifs for key transcriptional regulators.
This is a preview of subscription content, access via your institution
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 / 30 days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Rent or buy this article
Prices vary by article type
Prices may be subject to local taxes which are calculated during checkout
Liggett, L. A. & Sankaran, V. G. Cell 182, 1384–1400 (2020).
Fabre, M. A. et al. Nature 606, 335–342 (2022).
Koya, J. et al. Nat. Commun. 7, 10924 (2016).
Challen, G. A. et al. Nat. Genet. 44, 23–31 (2011).
Nam, A. S. et al. Nat. Genet. https://doi.org/.1038/s41588-022-01179-9 (2022).
Nam, A. S. et al. Nature 571, 355–360 (2019).
Ludwig, L. S. et al. Cell 176, 1325–1339.e22 (2019).
Xu, J. et al. eLife https://doi.org/10.7554/eLife.45105.001 (2019).
V.G.S. serves as an advisor to and/or has equity in Branch Biosciences, Ensoma, Novartis, Forma and Cellarity, all unrelated to the present work. The authors have no other competing interests to declare.
About this article
Cite this article
Voit, R.A., Sankaran, V.G. Multi-omics on our multitudes. Nat Genet 54, 1449–1450 (2022). https://doi.org/10.1038/s41588-022-01175-z