BIR-1, a Caenorhabditis elegans homologue of Survivin, regulates transcription and development

被引:11
作者
Kostrouchova, M
Kostrouch, Z
Saudek, V
Piatigorsky, J
Rall, JE
机构
[1] Charles Univ, Fac Med 1, Inst Inherited Metab Disorders, Lab Mol Biol & Genet, CZ-12801 Prague 2, Czech Republic
[2] Charles Univ, Fac Med 1, Inst Inherited Metab Disorders, Lab Mol Pathol, CZ-12801 Prague, Czech Republic
[3] NIDDK, Diabet Branch, NIH, Bethesda, MD 20892 USA
[4] NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1073/pnas.0730770100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
bir-1, a Caenorhabditis elegans inhibitor-of-apoptosis gene homologous to Survivin is organized in an operon with the transcription cofactor C elegans SKIP (skp-1). Because genes arranged in operons are frequently linked functionally, we have asked whether BIR-1 also functions in transcription. bir-1 inhibition resulted in multiple developmental defects that overlapped with C elegans SKIP loss-of-function phenotypes: retention of eggs, dumpy, movement defects, and lethality. bir-1 RNA-mediated interference decreased expression of several gfp transgenes and the endogenous genes dpy-7 and hlh-1. Immunoblot analysis revealed decreased phosphoacetylated histones in bir-1 RNA-mediated interference-treated worms. In a heterologous transfection system, BIR-1 augments thyroid hormone-regulated transcription and has an additive effect with SKIP. These results show that BIR-1 functions in the regulation of transcription and development.
引用
收藏
页码:5240 / 5245
页数:6
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