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Min, Kyung-Tai
Molecular & Cellular Neurobiology Lab(Min Lab)
Research Interests
  • adult neurogenesis; axon development; axon regeneration; protein stability; protein synthesis; Down syndrome; Alzheimer's disease;

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hnRNP Q regulates IRES-mediated fmr1 translation in neurons

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Title
hnRNP Q regulates IRES-mediated fmr1 translation in neurons
Author
Choi, Jung-HyunKim, Sung-HoonJeong, Young-HunKim, Sung WookMin, Kyung-TaiKim, Kyong-Tai
Issue Date
2019-02
Publisher
AMER SOC MICROBIOLOGY
Citation
MOLECULAR AND CELLULAR BIOLOGY, v.39, no.4, pp.e00371
Abstract
Fragile X syndrome (FXS) caused by loss of fragile X mental retardation protein (FMRP) is the most common cause of inherited intellectual disability. Numerous studies show that FMRP is a RNA binding protein that regulates translation of its binding targets and plays key roles in neuronal functions. However, the regulatory mechanism for FMRP expression is incompletely understood. Conflicting results regarding internal ribosome entry site (IRES)-mediated fmr1 translation were reported. Here, we unambiguously demonstrated that the fmr1 gene, which encodes FMRP, exploits both IRES-mediated translation and canonical cap-dependent translation. Furthermore, we found that heterogeneous nuclear ribonucleoprotein Q (hnRNP-Q) acts as IRES transacting factor (ITAF) for IRES-mediated fmr1 translation in neurons. We also showed that semaphorin 3A (Sema3A) induced axonal growth cone collapse is due to upregulation of hnRNP-Q and subsequent IRES-mediated expression of FMRP. These data elucidate the regulatory mechanism of FMRP expression and its role in axonal growth cone collapse.
URI
https://scholarworks.unist.ac.kr/handle/201301/25491
URL
https://mcb.asm.org/content/early/2018/11/21/MCB.00371-18
DOI
10.1128/MCB.00371-18
ISSN
0270-7306
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