Abstract
XNP/ATRX, a causative gene of X-linked alpha-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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Genetically Modified
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Apoptosis / genetics
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Apoptosis / physiology*
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Blotting, Northern
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Cell Cycle / genetics
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Cell Cycle / physiology
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DNA Helicases / genetics
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DNA Helicases / metabolism*
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Drosophila / genetics
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Drosophila / growth & development
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Drosophila / metabolism
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism*
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Enzyme Activation
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Eye / growth & development
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Eye / metabolism
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Eye / ultrastructure
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Female
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Gene Expression Regulation, Developmental
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In Situ Hybridization
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JNK Mitogen-Activated Protein Kinases / genetics
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JNK Mitogen-Activated Protein Kinases / metabolism*
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Male
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Microscopy, Electron, Scanning
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Microscopy, Fluorescence
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Mutation
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism*
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Reverse Transcriptase Polymerase Chain Reaction
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Wings, Animal / growth & development
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Wings, Animal / metabolism
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Wings, Animal / ultrastructure
Substances
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Drosophila Proteins
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Nuclear Proteins
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JNK Mitogen-Activated Protein Kinases
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DNA Helicases