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Jun and JunD-dependent functions in cell proliferation and stress response

Abstract : Jun is essential for fetal development, as fetuses lacking Jun die at mid-gestation with multiple cellular defects in liver and heart. Embryos expressing JunD in place of Jun (Jund/d) can develop to term with normal fetal livers, but display cardiac defects as observed in fetuses lacking Jun. Jund/d MEFs exhibit early senescence, which can be rescued by EGF and HB-EGF stimulation, probably through activation of Akt signaling. Thus, JunD can not functionally replace Jun in regulating fibroblast proliferation. In Jun-/- fetal livers increased H2O2 levels are detected and expression of Nrf1 and Nrf2 (nuclear erythroid 2-related transcription factors) is down regulated. Importantly, increased oxidative stress as well as expression of Nrf1 and Nrf2 is rescued by JunD in Jund/d fetal livers. These data demonstrate that Jun is of critical importance for cellular protection against oxidative stress in fetal livers and fibroblasts and Jun-dependent cellular senescence can be restored by activation of the EGFR pathway.
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Submitted on : Sunday, September 19, 2010 - 2:50:19 AM
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Erwin Wagner, Arabella Meixner, Florian Karreth, Lukas Kenner, Josef M Penninger. Jun and JunD-dependent functions in cell proliferation and stress response. Cell Death and Differentiation, Nature Publishing Group, 2010, n/a (n/a), pp.n/a-n/a. ⟨10.1038/cdd.2010.22⟩. ⟨hal-00519207⟩

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