한빛사 논문
Seokhwi Kim1, Nury Kim2, Jinsu Lee3, Sungsoo Kim3, Jongryul Hong3, Seungkyu Son3 and Won Do Heo2,3,4,*
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
2Center for Cognition and Sociality, Institute for Basic Science (IBS), Daejeon, Republic of Korea.
3Department of Biological Sciences, KAIST, Daejeon, Republic of Korea.
4KAIST Institute for the BioCentury, KAIST, Daejeon, Republic of Korea.
*Corresponding author.
Abstract
Activation of Fas (CD95) is observed in various neurological disorders and can lead to both apoptosis and prosurvival outputs, yet how Fas signaling operates dynamically in the hippocampus is poorly understood. The optogenetic dissection of a signaling network can yield molecular-level explanations for cellular responses or fates, including the signaling dysfunctions seen in numerous diseases. Here, we developed an optogenetically activatable Fas that works in a physiologically plausible manner. Fas activation in immature neurons of the dentate gyrus triggered mammalian target of rapamycin (mTOR) activation and subsequent brain-derived neurotrophic factor secretion. Phosphorylation of extracellular signal–regulated kinase (Erk) in neural stem cells was induced under prolonged Fas activation. Repetitive activation of this signaling network yielded proliferation of neural stem cells and a transient increase in spatial working memory in mice. Our results demonstrate a novel Fas signaling network in the dentate gyrus and illuminate its consequences for adult neurogenesis and memory enhancement.
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