BIR-1, the homologue of human Survivin, regulates expression of developmentally active collagen genes in C. elegans
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
17116281
PII: file/6158/fb2006a0013.pdf
Knihovny.cz E-zdroje
- MeSH
- Caenorhabditis elegans genetika růst a vývoj MeSH
- genetická transkripce MeSH
- geny helmintů genetika MeSH
- inhibitory apoptózy MeSH
- kolagen genetika MeSH
- larva metabolismus MeSH
- lidé MeSH
- mikročipová analýza MeSH
- nádorové proteiny metabolismus MeSH
- proteiny asociované s mikrotubuly metabolismus MeSH
- proteiny Caenorhabditis elegans metabolismus MeSH
- reprodukovatelnost výsledků MeSH
- RNA interference MeSH
- sekvenční homologie * MeSH
- stanovení celkové genové exprese MeSH
- survivin MeSH
- vývojová regulace genové exprese * MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- bir-1 protein, C elegans MeSH Prohlížeč
- BIRC5 protein, human MeSH Prohlížeč
- inhibitory apoptózy MeSH
- kolagen MeSH
- nádorové proteiny MeSH
- proteiny asociované s mikrotubuly MeSH
- proteiny Caenorhabditis elegans MeSH
- survivin MeSH
BIR-1 and Survivin are highly conserved members of the inhibitor of apoptosis protein family that regulate cell division in nematodes and mammals and inhibit apoptosis in mammals. In the C. elegans genome, bir-1 is organized in an operon together with transcription and splicing cofactor CeSKIP (skp-1) and is highly expressed during embryogenesis as well as in non-dividing cells during larval development. Previously we have shown that BIR-1 regulates transcription and development and its loss-of-function phenotype overlaps with loss of function of CeSKIP and nuclear hormone receptor CHR3 (NHR-23). Here we searched for genes whose expression is affected by BIR-1 loss of function using whole-genome microarray experiments and identified several collagen genes as candidate targets of bir-1 inhibition in L1 larval stage. The decreased expression of selected collagen genes in bir-l-inhibited larvae was confirmed by quantitative RT-PCR. Next, we generated transgenic lines expressing bir-1 mRNA under a heat shock-regulated promoter and tested whether bir-1 overexpression has the potential to augment the expression of genes that showed decreased expression in worms treated with bir-1 RNAi. Overexpression of bir-1 resulted in a pronounced increase (2 to 5 times) of the expression of these genes. Our findings support the concept that BIR-1, a protein generally regarded as a mitotic factor, is involved in the regulation of transcription during normal development of C. elegans and has a strong ability to affect transcription of developmentally active genes if overexpressed.