Abstract
Phosphatidylinositide 3 kinases (PI3Ks) and their downstream mediators AKT and mammalian target of rapamycin (mTOR) constitute the core components of the PI3K/AKT/mTOR signalling cascade, regulating cell proliferation, survival and metabolism. Although these functions are well-defined in the context of tumorigenesis, recent studies - in particular those using pluripotent stem cells - have highlighted the importance of this pathway to development and cellular differentiation. Here, we review the recent in vitro and in vivo evidence for the role PI3K/AKT/mTOR signalling plays in the control of pluripotency and differentiation, with a particular focus on the molecular mechanisms underlying these functions.
Highlights
During development, cellular differentiation is a crucial process by which all major tissues of the adult organism are formed
Distinct roles of mTOR complex 1 (mTORC1) and mTORC2 in embryonic development Given the key roles that mammalian target of rapamycin (mTOR) complexes play in AKT activation, protein translation and nucleotide biosynthesis, it is perhaps unsurprising to find that knockout mice of various components of the complexes lead to embryonic lethality (Rennebeck et al, 1998; Murakami et al, 2004; Guertin et al, 2006; Shiota et al, 2006; Jacinto et al, 2006; Goorden et al, 2011)
Phosphatidylinositide 3 kinases (PI3Ks)/AKT/mTOR signalling in pluripotent stem cells in vivo studies have been informative in terms of establishing a role for PI3K/AKT/mTOR signalling in the regulation of early embryonic development, the inherent complexity and multiple layers of redundancy present a formidable barrier to the elucidation of the molecular details involved
Summary
Cellular differentiation is a crucial process by which all major tissues of the adult organism are formed. Distinct roles of mTORC1 and mTORC2 in embryonic development Given the key roles that mTOR complexes play in AKT activation, protein translation and nucleotide biosynthesis, it is perhaps unsurprising to find that knockout mice of various components of the complexes lead to embryonic lethality (Rennebeck et al, 1998; Murakami et al, 2004; Guertin et al, 2006; Shiota et al, 2006; Jacinto et al, 2006; Goorden et al, 2011).
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