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c-Fos Activated Phospholipid Synthesis Is Required for Neurite Elongation in Differentiating PC12 CellsD⃞

机译:分化PC12细胞中神经突延伸需要c-Fos激活的磷脂合成

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摘要

We have previously shown that c-Fos activates phospholipid synthesis through a mechanism independent of its genomic AP-1 activity. Herein, using PC12 cells induced to differentiate by nerve growth factor, the genomic effect of c-Fos in initiating neurite outgrowth is shown as distinct from its nongenomic effect of activating phospholipid synthesis and sustaining neurite elongation. Blocking c-Fos expression inhibited differentiation, phospholipid synthesis activation, and neuritogenesis. In cells primed to grow, blocking c-Fos expression determined neurite retraction. However, transfected cells expressing c-Fos or c-Fos deletion mutants with capacity to activate phospholipid synthesis sustain neurite outgrowth and elongation in the absence of nerve growth factor. Results disclose a dual function of c-Fos: it first releases the genomic program for differentiation and then associates to the endoplasmic reticulum and activates phospholipid synthesis. Because phospholipids are key membrane components, we hypothesize this latter phenomenon as crucial to support membrane genesis demands required for cell growth and neurite elongation.
机译:先前我们已经证明c-Fos通过独立于其基因组AP-1活性的机制激活磷脂合成。在本文中,使用由神经生长因子诱导分化的PC12细胞,c-Fos在启动神经突生长中的基因组作用与激活磷脂合成并维持神经突延长的非基因组作用不同。阻断c-Fos表达可抑制分化,磷脂合成激活和神经形成。在准备生长的细胞中,阻断c-Fos表达决定了神经突回缩。然而,在不存在神经生长因子的情况下,表达具有激活磷脂合成能力的c-Fos或c-Fos缺失突变体的转染细胞维持了神经突的生长和伸长。结果揭示了c-Fos的双重功能:它首先释放用于分化的基因组程序,然后与内质网缔合并激活磷脂合成。由于磷脂是关键的膜成分,因此我们认为后一种现象对于支持细胞生长和神经突伸长所需的膜起源需求至关重要。

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