Clonal Tracing with Somatic Epimutations Reveals Dynamics of Blood Ageing

Clonal tracing with somatic epimutations reveals dynamics of blood ageing

Current approaches used to track stem cell clones through differentiation require genetic engineering1,2 or rely on sparse somatic DNA variants3,4, which limits their wide application. Here we discover that DNA methylation of a subset of CpG sites reflects cellular differentiation, whereas another subset undergoes stochastic epimutations and can serve as digital barcodes of clonal identity. We demonstrate that targeted single-cell profiling of D…

‘Barcodes’ in the DNA could prevent disease and slow down ageing, researchers say

The discovery could offer a new understanding of how blood ages over time

One in two living people will develop a blood-related disease. They will be mainly cardiovascular ailments, but also cancer or deficiencies of the immune system. It is a calculation made by molecular biologist Lars Velten, who works at the Centre for Genomic Regulation in Barcelona trying to unravel the many riddles that still exist about how blood evolves as we age and why some people will suffer those life-threatening diseases and others will …

DNA ‘barcodes’ shed light on how the blood ages

The discovery could help prevent diseases years before symptoms appear, as well as paving the way for the exploration of rejuvenation therapies.

'Barcodes' written into DNA reveal how blood ages

A study in the journal Nature explains how age reshapes the blood system. In both humans and mice, a few stem cells, or "clones," outcompete their neighbors and gradually take over blood production. The blood stem cell reservoir shrinks and becomes dominated by clones which show a preference for producing myeloid cells, immune cells linked to chronic inflammation.

The discovery, important for anti-aging and signed by scientists from the Center for Genomic Regulation (CRG) and the Institute for Biomedical Research (IRB Barcelona), was possible after a study with donors of marrow and mice. In both of them, blood stem cells age reducing their diversity and favoring associated types or “clones” that lead to chronic inflammation, changes that are “almost universal” from the age of 60.