dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons

Mutation of the XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-06, Vol.384 (2), p.160-166
Main Authors: Hong, Yoon Ki, Lee, Nam Gon, Lee, Min Jung, Park, Min Soo, Choi, Gahee, Suh, Yoon Seak, Han, Seung Yeop, Hwang, Soojin, Jeong, Gilsang, Cho, Kyoung Sang
Format: Article
Language:English
Subjects:
Animals
Apoptosis
ATRX
Caspases - metabolism
dFOXO
DNA Helicases
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Drosophila
Drosophila melanogaster - cytology
Drosophila melanogaster - genetics
Drosophila melanogaster - growth & development
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
dXNP
Forkhead Transcription Factors - metabolism
JNK
JNK Mitogen-Activated Protein Kinases - metabolism
Neurogenesis - genetics
Neuronal development
Neurons - enzymology
Neurons - physiology
Neuropeptides - genetics
Transcription, Genetic
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Summary:Mutation of the XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet to be determined. To better understand the role of XNP/ATRX in neuronal development, we expressed Drosophila XNP ( dXNP/DATRX) ectopically in Drosophila neurons. Neuronal expression of dXNP/DATRX resulted in various developmental defects and induced strong apoptosis. These defects and apoptosis were suppressed by Drosophila inhibitor of apoptosis protein 1. Expression of dXNP/DATRX also increased JNK activity and the levels of reaper and hid transcripts, which are pro-apoptotic factors that activate caspase. Furthermore, dXNP/DATRX-induced rough eye phenotype and apoptosis were suppressed by dFOXO deficiency. These results suggest that dXNP/DATRX is involved in caspase-dependent apoptosis in Drosophila neurons via regulation of the JNK and dFOXO pathway.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.04.112