dXNP, a Drosophila homolog of XNP/ATRX, induces apoptosis via Jun-N-terminal kinase activation

Lee, Nam Gon; Hong, Yoon Ki; Yu, Si Young; Han, Seung Yeop; Geum, Dongho; Cho, Kyoung Sang

Abstract: XNP/ATRX, a causative gene of X-linked α-thalassemia/mental retardation syndrome, encodes an SNF2 family ATPase/helicase protein. To better understand the role of XNP/ATRX in development, we isolated and characterized a Drosophila XNP/ATRX homolog, dXNP, which contains highly conserved SNF2 and helicase domains. Ectopically expressed dXNP induced strong apoptosis in the developing eye and wing, but did not affect cell cycle progression or the expression of wingless and engrailed, essential regulators of development. The dXNP-induced apoptosis was strongly suppressed by DJNKK/hemipterous mutation, and dXNP increased JNK activity. Taken together, these results suggest that dXNP regulates apoptosis via JNK activation.

DROSOPHILA; INTELLECTUAL disabilities; CELL death; APOPTOSIS

FEBS Letters, 2007, Vol 581, Issue 14, p2625

0014-5793

Academic Journal

10.1016/j.febslet.2007.05.005