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Mol. Cells 2010; 29(6): 575-580

Published online June 30, 2010

https://doi.org/10.1007/s10059-010-0068-1

© The Korean Society for Molecular and Cellular Biology

Parkin Suppresses c-Jun N-Terminal Kinase-Induced Cell Death via Transriptional Regulation in Drosophila

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

Received: January 19, 2010; Accepted: February 10, 2010

Abstract

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

Article

Research Article

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.

Parkin Suppresses c-Jun N-Terminal Kinase-Induced Cell Death via Transriptional Regulation in Drosophila

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

Received: January 19, 2010; Accepted: February 10, 2010

Abstract

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
May 31, 2022 Vol.45 No.5, pp. 273~352
COVER PICTURE
Fe2+ ion depletion-induced expression of BΔGFP at the early stage of leaf development (Choi et al., pp. 294-305).

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