FoxO limits microtubule stability and is itself negatively regulated by microtubule disruption.
Bottom Line: Indeed, levels of neuronal FoxO were strongly reduced after acute pharmacological MT disruption as well as sustained genetic disruption of the neuronal cytoskeleton.This decrease was independent of the dual leucine zipper kinase-Wallenda pathway and required function of Akt kinase.We present a model wherein FoxO degradation is a component of a stabilizing, protective response to cytoskeletal insult.
Affiliation: Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106, USA.Show MeSH
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Mentions: foxO was identified in a misexpression screen for genes involved in motor neuron differentiation. An upstream activation sequence (UAS)–containing P element, GS1664, inserted upstream of the foxO gene, disrupts the embryonic axonal scaffold when crossed to the panneuronal driver ElavGal4 (Fig. 1 C and not depicted). The phenotype is attributable to elevated FoxO levels, as ElavGal4-driven overexpression of a UAS-foxOWT transgene yields an equivalent phenotype (Fig. 1, A and B).
Affiliation: Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106, USA.