Excess protein synthesis in Drosophila fragile X mutants impairs long-term memory.

Excess protein synthesis in Drosophila fragile X mutants impairs long-term memory.
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DOI:
10.1038/nn.2175
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发表时间:
2008-10
影响因子:
25
通讯作者:
Tully, Tim
Tully, Tim
中科院分区:
医学1区
文献类型:
--
作者:
Bolduc, Francois V.;Bell, Kimberly;Cox, Hilary;Broadie, Kendal S.;Tully, Tim

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我们使用果蝇的嗅觉记忆,以了解在体内脆性X综合征认知缺陷的分子基础。我们观察到脆性X蛋白(FMRP)在长时记忆(LTM)中是急性需要的,并与argonaute1和staufen相互作用。脆性X突变体中长期记忆形成的阻断可以通过蛋白质合成抑制剂来挽救,这表明过量的基线蛋白质合成可能对认知产生负面影响。
We used Drosophila olfactory memory in order to understand in vivo the molecular basis of cognitive defect in Fragile X syndrome. We observed that Fragile X protein (FMRP) was required acutely and interacted with argonaute1 and staufen in long-term memory (LTM). Occlusion of long-term memory formation in Fragile X mutants could be rescued by protein synthesis inhibitors, suggesting that excess baseline protein synthesis could impact negatively on cognition.
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