Elucidation of a mechanism of ALS system selectivity focusing on TDP-43 function in interneurons.
| Project/Area Number |
15K19479
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ALS / スプライシング / 介在ニューロン / stasimon / iPS細胞 |
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| Outline of Final Research Achievements |
We aimed to elucidate the mechanism of the pathogenesis of amyotrophic lateral sclerosis (ALS). We have already reported the decrease of the main component of splicing machinery, U snRNAs and GEM bodies, and several aberrant splicing in ALS affected tissues.
In this study, we intended to clarify the role of interneurons in ALS and its RNA metabolism disorder. We found that it is necessary to pay attention to RNA fragmentation in the isolation and quantification of mRNA from formalin-fixed paraffin-embedded tissue. Furthermore, we focused on stasimon mRNA splicing which was reported as a cause of motor neuron degeneration mediated by interneurons disability in spinal muscular atrophy model animals, and confirmed the same splicing mutation in TDP-43 expression suppressing cells.
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Report
(3 results)
Research Products
(9 results)
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[Journal Article] Increased cytoplasmic TARDBP mRNA in affected spinal motor neurons in ALS caused by abnormal autoregulation of TDP-43.2016
Author(s)
Koyama A, Sugai A, Kato T, Ishihara T, Shiga A, Toyoshima Y, Koyama M, Konno T, Hirokawa S, Yokoseki A, Nishizawa M, Kakita A, Takahashi H, Onodera O.
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Journal Title
Nucleic Acids Res
Volume: 44
Issue: 12
Pages: 5820-5836
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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