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

作者：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^*

来源：Biochemical and Biophysical Research Communications, 2009, 384(2): 160-166.

DOI：10.1016/j.bbrc.2009.04.112

• Apoptosis
• ATRX
• Drosophila
• dXNP
• dFOXO
• JNK
• Neuronal development

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.

• 出版日期2009-6-26