Category: Parkinson's Disease: Pathophysiology
Objective: Our study proposes a novel regulator for the protection of TAF15-induced proteinopathy and adds to our understanding of the exact pathogenic mechanism for TAF15-induced neurodegeneration.
Background: Parkinson’s disease (PD) is the second most common neurodegenerative brain disease and we have known both genetic and environmental factors contribute to the development of PD. And a rare recessive form of the disease may be caused by a mutation in the PARK2 gene, whose product, Parkin, controls mitophagy and programmed cell death. Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder which is characterized pathologically by the loss of motor neurons. Previous studies regarding ALS-related factors included discussion of the FET-protein family (consisting of FUS, EWS and TAF15), which are Fe(II) and α-ketoglutarate (α-KG)-dependent ten-eleven translocation (TET) enzymes; this protein family catalyzes oxidation and decarboxylation, and is involved in transcriptional regulation, mRNA splicing and polyadenylation, RNA transport, RNA translation and microRNA (miRNA) processing.
Method: A. Drosophila stocks.
B. Western blot analysis.
C. Immunohistochemistry.
D. Blue native polyacrylamide gel electrophoresis (BN-PAGE).
E. ATP assay.
Results: 1. Parkin is a novel binding partner and regulator for TAF15 in Drosophila
2. The necrotic plaques in parkin RNAi and TAF15 co-expressing flies were severely increased in an age-dependent manner
Conclusion: In this study, it was to identify a novel regulator for protection from neurotoxicity and to further understand the protective mechanism against a TAF15-induced proteinopathy, using genetic and molecular experimental approaches in Drosophila. Parkin overexpression during aging has been shown to decrease proteotoxicity. Our study provides in vivo evidence supporting the use of parkin for neuroprotection in TAF15-induced proteinopathy and new insights into the pathogenic mechanisms
To cite this abstract in AMA style:
E.J Choi, D.G Lee, CC. Cui, K.Y Kim. The interaction of Parkin and TAF15 for the Drosophila in which neuronal defect was induced [abstract]. Mov Disord. 2020; 35 (suppl 1). https://www.mdsabstracts.org/abstract/the-interaction-of-parkin-and-taf15-for-the-drosophila-in-which-neuronal-defect-was-induced/. Accessed May 10, 2025.« Back to MDS Virtual Congress 2020
MDS Abstracts - https://www.mdsabstracts.org/abstract/the-interaction-of-parkin-and-taf15-for-the-drosophila-in-which-neuronal-defect-was-induced/