Novel view of the adult stem cell compartment – of germline and parental imprinting

Abstract

Evidence has accumulated that adult tissues contain developmentally early stem cells that remain in a dormant state as well as stem cells that are more proliferative, supplying tissue-specific progenitor cells and thus playing a more active role in the turnover of adult tissues. Interestingly, evidence has accumulated in parallel that these most primitive, dormant, adult stem cells are regulated by epigenetic changes in the expression of certain parentally imprinted genes, a molecular phenomenon previously described for keeping primordial germ cells in a quiescent state. Specifically, the most primitive quiescent stem cells in bone marrow that can be committed to the hematopoietic lineage show erasure of imprinting at the Igf2-H19 locus, which keeps them in a quiescent state in a similar manner as primordial germ cells. Similar changes in expression of parentally imprinted genes may also play a role in the quiescence of dormant adult stem cells present in other non-hematopoietic tissues. However, this possibility requires further study.

Why are hematopoietic stem cells so ‘sexy’? on a search for developmental explanation

“…11,31 While post-migrating PGCs ultimately establish gametogenesis, early PGCs, which I will discuss below, could theoretically give rise to hemangioblasts and initiate primitive hematopoiesis in the yolk sac blood islands, and late-migratory PGCs could give rise to definitive hematopoiesis in the AGM region, where the first HSCs can be identified that are associated with the aortic endothelium. 30–32 …”

“…2,34 However, this concept that HSCs from the yolk sac may specify into definitive HSCs and colonize aortic endothelium, does not preclude the possibility that the aortic endothelium could be colonized by PGC-derived cells migrating through the AGM region by 11 dpc in mice. 30–32 For the initiation of definitive hematopoiesis in the aortic endothelium, it is known that there is an effect induced by shear forces from active blood flow. 35 Again, we cannot preclude that these shear forces act on migrating PGC-derived cells that infiltrate the aortic endothelium.…”