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J Dev Biol June 1, 2016; 4 (2):
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Nutrient-Deprived Retinal Progenitors Proliferate in Response to Hypoxia: Interaction of the HIF-1 and mTOR Pathway.

Khaliullina H , Love NK , Harris WA .

At a cellular level, nutrients are sensed by the mechanistic Target of Rapamycin (mTOR). The response of cells to hypoxia is regulated via action of the oxygen sensor Hypoxia-Inducible Factor 1 (HIF-1). During development, injury and disease, tissues might face conditions of both low nutrient supply and low oxygen, yet it is not clear how cells adapt to both nutrient restriction and hypoxia, or how mTOR and HIF-1 interact in such conditions. Here we explore this question in vivo with respect to cell proliferation using the ciliary marginal zone (CMZ) of Xenopus. We found that both nutrient-deprivation and hypoxia cause retinal progenitors to decrease their proliferation, yet when nutrient-deprived progenitors are exposed to hypoxia there is an unexpected rise in cell proliferation. This increase, mediated by HIF-1 signalling, is dependent on glutaminolysis and reactivation of the mTOR pathway. We discuss how these findings in non-transformed tissue may also shed light on the ability of cancer cells in poorly vascularised solid tumours to proliferate.

PubMed ID: 27280081
PMC ID: PMC4894462
Article link: J Dev Biol
Grant support: [+]

Species referenced: Xenopus
Genes referenced: arnt ccdc34 h3-3a hif1a mtor rps6
GO keywords: cell proliferation involved in compound eye morphogenesis [+]
Antibodies: Rps6 Ab3

Phenotypes: Xl Wt + nutrient deprivation + hypoxia + Echinomycin [+]

Article Images: [+] show captions
References [+] :
Agathocleous, Metabolism in physiological cell proliferation and differentiation. 2013, Pubmed