title: Induction of fusion-competent myoblast-specific gene expression during myogenic differentiation of Drosophila Schneider cells by DNA double-strand breaks or replication inhibition.
abstract: Differentiation of Drosophila Schneider cells caused by DNA double-strand break (DSB)-inducing topoisomerase II (topo II) inhibitors were attenuated by ICRF-193, a non-DNA-damaging topo II inhibitor. ICRF-193 did not inhibit differentiation induced by neocarzinostatin (NCS), a drug that causes DNA DSBs independent of topo II. Schneider cells differentiated upon treatment with gamma-ray. These results suggest that DNA DSBs induce myogenic differentiation of Schneider cells. We also found DNA replication inhibitors, hydroxyurea (HU), aphidicolin, and ethylmethanesulfonate (EMS) induced myogenic differentiation of Schneider cells. HU-induced differentiation was inhibited upon pretreatment of cells with chemical inhibitors of PP 1/2A, p38 MAPK, JNK, and proteasome. RT-PCR analysis revealed that the expressions of fusion-competent myoblast-specific genes lmd, sns, and del were induced in Schneider cells upon treatment with NCS or HU, whereas expressions of three founder cell-specific genes, duf, ants, and rols, were undetectable. These results indicate that the expression of fusion competent-myoblast-specific genes is induced during myogenic differentiation of Drosophila Schneider cells by DNA DSBs or replication inhibition.
authors.affiliation: Laboratory of Developmental Biochemistry, Faculty of Pharmaceutical Sciences, The University of Tokyo, 3-1, 7-Chome, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
authors.forename: Muktadir S
authors.initials: MS
authors.lastname: Hossain
authors.forename: Kenji
authors.initials: K
authors.lastname: Kurokawa
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Sekimizu
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D016590:Aphidicolin / Q000494:pharmacology; D002454:Cell Differentiation; D002460:Cell Line; D004247:DNA / Q000378:metabolism; D004249:DNA Damage; D004261:DNA Replication; D054659:Diketopiperazines; D004330:Drosophila; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D005720:Gamma Rays; D006918:Hydroxyurea / Q000494:pharmacology; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D048670:MAP Kinase Kinase 4; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D009132:Muscles / Q000166:cytology; D032446:Myoblasts / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000378:metabolism; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013997:Time Factors; D059005:Topoisomerase II Inhibitors; D009353:Zinostatin / Q000494:pharmacology; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D054659:Diketopiperazines; D004791:Enzyme Inhibitors; D019384:Nucleic Acid Synthesis Inhibitors; D010879:Piperazines; D059005:Topoisomerase II Inhibitors; C070899:4,4'-(1,2-dimethyl-1,2-ethanediyl)bis-2,6-piperazinedione; D016590:Aphidicolin; D004247:DNA; D009353:Zinostatin; D005020:Ethyl Methanesulfonate; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4; D020929:Mitogen-Activated Protein Kinase Kinases; D046988:Proteasome Endopeptidase Complex; D018995:Myosin Heavy Chains; D006918:Hydroxyurea