Mol. Cells 2010; 29(6): 575-580
Published online May 20, 2010
https://doi.org/10.1007/s10059-010-0068-1
© The Korean Society for Molecular and Cellular Biology
Correspondence to : *Correspondence: kscho@konkuk.ac.kr
Parkin is the most prevalent genetic factor in the onset of autosomal recessive juvenile parkinsonism (AR-JP), and mutations in parkin has been reported to cause motor defects, which result from dopamine deficiency caused by dopaminergic neuronal cell death. Activation of c-Jun N-terminal kinase (JNK) has also been implicated in neuronal cell death in Parkinson’s disease (PD). Moreover, Droso-phila models for AR-JP, loss of function mutants of Dro-sophila parkin, also show dopaminergic neural degenera-tion associated with hyperactivation of JNK, increased apoptosis, and mitochondrial defects. However, the molecular mechanism by which Parkin protects cells from apoptosis remains unclear. In the present study, we tested whether Drosophila Parkin suppressed the JNK signaling pathway in developing tissues. Ectopically expressed parkin strongly suppressed the constitutively active form of Hemipterous (HepCA), a Drosophila JNK kinase that induces an eye degeneration phenotype and apoptosis in the eye imaginal disc. Moreover, parkin also suppressed extra vein formation induced by Basket (Bsk), a Drosophila JNK. Interestingly, the bsk mRNA level was markedly reduced by parkin over-expression, suggesting that the effect of parkin on the phenotype induced by activation of JNK signaling was achieved by transcriptional regulation. Furthermore, we found that the expression level of JNK target genes was reduced by parkin over-expression. Taken together, these results suggest that Drosophila Parkin suppresses JNK signaling by reducing bsk transcription.
Keywords flooding, apoptosis, bsk, hep, JNK, Parkin, Parkinson’s disease
Mol. Cells 2010; 29(6): 575-580
Published online June 30, 2010 https://doi.org/10.1007/s10059-010-0068-1
Copyright © The Korean Society for Molecular and Cellular Biology.
Soojin Hwang1, Darae Kim1, Gahee Choi, Seon Woo An, Yoon Ki Hong, Yoon Seak Suh, Min Jung Lee,
and Kyoung Sang Cho*
Department of Biological Sciences, Konkuk University, Seoul 143-701, Korea, 1The authors equally contributed to this work.
Correspondence to:*Correspondence: kscho@konkuk.ac.kr
Parkin is the most prevalent genetic factor in the onset of autosomal recessive juvenile parkinsonism (AR-JP), and mutations in parkin has been reported to cause motor defects, which result from dopamine deficiency caused by dopaminergic neuronal cell death. Activation of c-Jun N-terminal kinase (JNK) has also been implicated in neuronal cell death in Parkinson’s disease (PD). Moreover, Droso-phila models for AR-JP, loss of function mutants of Dro-sophila parkin, also show dopaminergic neural degenera-tion associated with hyperactivation of JNK, increased apoptosis, and mitochondrial defects. However, the molecular mechanism by which Parkin protects cells from apoptosis remains unclear. In the present study, we tested whether Drosophila Parkin suppressed the JNK signaling pathway in developing tissues. Ectopically expressed parkin strongly suppressed the constitutively active form of Hemipterous (HepCA), a Drosophila JNK kinase that induces an eye degeneration phenotype and apoptosis in the eye imaginal disc. Moreover, parkin also suppressed extra vein formation induced by Basket (Bsk), a Drosophila JNK. Interestingly, the bsk mRNA level was markedly reduced by parkin over-expression, suggesting that the effect of parkin on the phenotype induced by activation of JNK signaling was achieved by transcriptional regulation. Furthermore, we found that the expression level of JNK target genes was reduced by parkin over-expression. Taken together, these results suggest that Drosophila Parkin suppresses JNK signaling by reducing bsk transcription.
Keywords: flooding, apoptosis, bsk, hep, JNK, Parkin, Parkinson’s disease
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