I read paper "Wnt signaling controls the specification of definitive and primitive hematopoiesis from human pluripotent stem cells"----I confused that why primitive do not have T lymphoid potential?(the fetal T cells are from definitive HSC? )
salam alikum
You can see this artical by Christopher M. Sturgeon , Which discussed Efforts to derive hematopoietic stem cells (HSCs) from human pluripotent stem cells (hPSCs) are complicated by the fact that embryonic hematopoiesis consists of two programs, primitive and definitive, that differ in developmental potential. As only definitive hematopoiesis generates HSCs, understanding how this program develops is essential for being able to produce this cell population in vitro. Here we show that both hematopoietic programs transition through hemogenic endothelial intermediates and develop from KDR+CD34−CD144− progenitors that are distinguished by CD235a expression. Generation of primitive progenitors (KDR+CD235a+) depends on stage-specific Activin-nodal signaling and inhibition of the Wnt-β-catenin pathway,whereas specification of definitive progenitors (KDR+CD235a−) requires Wnt-β-catenin signaling during this same time frame. Together, these findings establish simple selective differentiation strategies for the generation of primitive or definitive hematopoietic progenitors via Wnt-β-catenin manipulation, and in doing so provide access to enriched populations for future studies on hPSCderived hematopoietic development.
Good Luck
I don't think "primitive vs. definitive" is a particularly high resolution model. It has its historic origins in red cell hemoglobin switching, and may be useful for those cells.
When speaking about HSC, I'd rather break it down in terms of Aortic vs. Fetal Liver vs. Bone-marrow stages. In order to be a long-term transplantable HSC, it must have multilineage potential, self-renewal, and bone-marrow homing.
Only adult-type, bone marrow HSC have those three characteristics together. We don't presently know which markers might distinguish those cells from their non-transplantable, more primitive precursors.
No, AGM cells aren't considered "transplantable" into adult animals. They lack bone-marrow homing receptors, and probably also have a lineage potential that's somewhat off (more myelo, less lympho).
AGM HSC can home to fetal liver, which is the next logical developmental step for them. I think they go that route when transplanted into newborns.
It means HSC in YS, AGM, liver are immature（can not support the long term blood replacement）only BM can support the maturation of HSC. So if i want to derive HSC from HES, I must make sure those cells have the ability to migrate to BM. (expression some ligands can be recognized by BM). Or maybe someone could build a maturation system in vitro?
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