AI Article Synopsis
- Almost every time a mammalian cell divides, there’s a chance that mutations occur, leading to genetically different cells within the organism.
- These variations become fixed and can multiply into distinct cell clones, creating a complex genetic landscape in mammals.
- Recent studies show that these genetic variations can grow with age, impact how tissues function, and play a role in disease, highlighting the need for more research to understand their clinical significance.
Article Abstract
Nearly every mammalian cell division is accompanied by a mutational event that becomes fixed in a daughter cell. When carried forward to additional cell progeny, a clone of variant cells can emerge. As a result, mammals are complex mosaics of clones that are genetically distinct from one another. Recent high-throughput sequencing studies have revealed that mosaicism is common, clone sizes often increase with age and specific variants can affect tissue function and disease development. Variants that are acquired during early embryogenesis are shared by multiple cell types and can affect numerous tissues. Within tissues, variant clones compete, which can result in their expansion or elimination. Embryonic mosaicism has clinical implications for genetic disease severity and transmission but is likely an under-recognized phenomenon. To better understand its implications for mosaic individuals, it is essential to leverage research tools that can elucidate the mechanisms by which expanded embryonic variants influence development and disease.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11408116 | PMC |
| http://dx.doi.org/10.1038/s41576-024-00715-z | DOI Listing |
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