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First published online April 24, 2006

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CTCF shuttle puts brakes on growth

CTCF is a transcription factor that is thought to function as a tumor suppressor. It has been implicated in regulation of cell growth, differentiation and apoptosis, but the basis for the growth-suppressing ability that marks it as a potential tumor suppressor has been unclear. On p. 1746, Dolores Delgado and co-workers show that targeting of CTCF to the nucleolus might be crucial. They find that shuttling of CTCF from the nucleoplasm to the nucleolus correlates with growth arrest: in K562 myeloid cells, it is associated with differentiation; in MCF7 breast cancer cells, it is associated with apoptosis. They go on to show that this requires the central Zn-finger domain in CTCF and depends on active transcription by RNA polymerase I. Finally, the authors demonstrate that CTCF inhibits nucleolar transcription and that this is regulated by poly(ADP-ribosyl)ation of the protein. They suggest that translocation of CTCF to the nucleolus is needed to sustain metabolic changes necessary for growth arrest. Since poly(ADP-ribosyl) polymerases (PARPs) are present in nucleoli and regulate numerous nuclear processes, CTCF may function as part of a network of PARP effectors.

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Targeting of CTCF to the nucleolus inhibits nucleolar transcription through a poly(ADP-ribosyl)ation-dependent mechanism

Verónica Torrano, Joaquín Navascués, France Docquier, Ru Zhang, Les J. Burke, Igor Chernukhin, Dawn Farrar, Javier León, María T. Berciano, Rainer Renkawitz, Elena Klenova, Miguel Lafarga, and M. Dolores Delgado
JCS 2006 119: 1746-1759. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content