Degradation of high affinity HuD targets releases Kv1.1 mRNA from miR-129 repression by mTORC1

Author:

Sosanya Natasha M.1,Huang Peggy P.C.1,Cacheaux Luisa P.1,Chen Chun Jung1,Nguyen Kathleen2,Perrone-Bizzozero Nora I.3,Raab-Graham Kimberly F.1

Affiliation:

1. Center for Learning and Memory, Section of Neurobiology; and Section of Molecular Genetics and Microbiology; University of Texas at Austin, Austin, TX 78712

2. College of Medicine, Texas A&M Health Science Center, Bryan, TX 77807

3. Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131

Abstract

Little is known about how a neuron undergoes site-specific changes in intrinsic excitability during neuronal activity. We provide evidence for a novel mechanism for mTORC1 kinase–dependent translational regulation of the voltage-gated potassium channel Kv1.1 messenger RNA (mRNA). We identified a microRNA, miR-129, that repressed Kv1.1 mRNA translation when mTORC1 was active. When mTORC1 was inactive, we found that the RNA-binding protein, HuD, bound to Kv1.1 mRNA and promoted its translation. Unexpectedly, inhibition of mTORC1 activity did not alter levels of miR-129 and HuD to favor binding to Kv1.1 mRNA. However, reduced mTORC1 signaling caused the degradation of high affinity HuD target mRNAs, freeing HuD to bind Kv1.1 mRNA. Hence, mTORC1 activity regulation of mRNA stability and high affinity HuD-target mRNA degradation mediates the bidirectional expression of dendritic Kv1.1 ion channels.

Publisher

Rockefeller University Press

Subject

Cell Biology

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