Abstract
BackgroundThe quaking viable (qkv) mouse has several developmental defects that result in rapid tremors in the hind limbs. The qkI gene expresses three major alternatively spliced mRNAs (5, 6 and 7 kb) that encode the QKI-5, QKI-6 and QKI-7 RNA binding proteins that differ in their C-terminal 30 amino acids. The QKI isoforms are known to regulate RNA metabolism within oligodendrocytes, however, little is known about their roles during cellular stress.Methodology/Principal FindingsIn this study, we report an interaction between the QKI-6 isoform and a component of the RNA induced silencing complex (RISC), argonaute 2 (Ago2). We show in glial cells that QKI-6 co-localizes with Ago2 and the myelin basic protein mRNA in cytoplasmic stress granules.ConclusionsOur findings define the QKI isoforms as Ago2-interacting proteins. We also identify the QKI-6 isoform as a new component of stress granules in glial cells.
Highlights
The quaking viable mice represent an animal model with dysmyelination defects in the central and peripheral nervous system (CNS, PNS) [1]
We identify the QKI-6 isoform as a new component of stress granules in glial cells
We show that QKI-6 co-localizes with argonaute 2 (Ago2), PABP1, TIA1 and myelin basic protein (MBP) mRNA in stress granules in glial cells
Summary
The quaking viable (qkv) mice represent an animal model with dysmyelination defects in the central and peripheral nervous system (CNS, PNS) [1]. The genetic defect of the qkv mice has been linked to the qkI gene known to express 3 major alternatively spliced mRNAs of 5, 6 and 7 kb [3]. These mRNAs encode QKI-5, QKI-6 and QKI-7 respectively, which differ in their C-terminal 30 amino acids. It is thought that the inadequate expression of QKI-6 and QKI-7 causes the lack of oligodendrocyte maturation and the dysmyelination defects observed in qkv mice [6]. The QKI isoforms are known to regulate RNA metabolism within oligodendrocytes, little is known about their roles during cellular stress
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