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<p>mRNA translational repression by eukaryotic initiation factor 4E-binding proteins (4E-BPs), plays a critical role in synaptic plasticity and the formation of long-term memory (LTM). Among the three 4E-BP paralogs, 4E-BP2 is the predominant form expressed in neurons, and its full-body deletion in mice causes memory deficits. Mice lacking 4E-BP2 in GABAergic inhibitory interneurons, but not excitatory neurons, display autistic-like behaviors and deficits in object location and recognition. The specific mRNAs translationally regulated by 4E-BP2 in GABAergic interneurons, and how they contribute to spatial and associative memory, are unknown. Here, we show that conditional knockout (cKO) mice lacking 4E-BP2 selectively in GABAergic interneurons exhibit impairments in long-term spatial and contextual fear memory formation. We further demonstrate that 4E-BP2 deletion controls the translation of selective mRNAs in interneurons without increasing general protein synthesis. One of the mRNAs is <i>Gal</i>, which encodes a neuropeptide that modulates memory. Our findings provide evidence that 4E-BP2 selectively controls the translation of a subset of mRNAs in inhibitory neurons that are required for LTM formation.</p>

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4E-BP2-dependent translational control in GABAergic interneurons is required for long-term memory

  • 期刊论文

  • 发表日期：

    2026年1月30日

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  • Ziying Huang,
  • Niaz Mahmood,
  • Konstantina Psycharis,
  • Kevin Lister,
  • Mehdi Hooshmandi,
  • Nikhil Nageshwar Inturi,
  • Diana Tavares-Ferreira,
  • Shane Wiebe,
  • Arkady Khoutorsky,
  • Nahum Sonenberg

摘要

mRNA translational repression by eukaryotic initiation factor 4E-binding proteins (4E-BPs), plays a critical role in synaptic plasticity and the formation of long-term memory (LTM). Among the three 4E-BP paralogs, 4E-BP2 is the predominant form expressed in neurons, and its full-body deletion in mice causes memory deficits. Mice lacking 4E-BP2 in GABAergic inhibitory interneurons, but not excitatory neurons, display autistic-like behaviors and deficits in object location and recognition. The specific mRNAs translationally regulated by 4E-BP2 in GABAergic interneurons, and how they contribute to spatial and associative memory, are unknown. Here, we show that conditional knockout (cKO) mice lacking 4E-BP2 selectively in GABAergic interneurons exhibit impairments in long-term spatial and contextual fear memory formation. We further demonstrate that 4E-BP2 deletion controls the translation of selective mRNAs in interneurons without increasing general protein synthesis. One of the mRNAs is Gal, which encodes a neuropeptide that modulates memory. Our findings provide evidence that 4E-BP2 selectively controls the translation of a subset of mRNAs in inhibitory neurons that are required for LTM formation.