The cell-cycle regulator geminin inhibits Hox function through direct and polycomb-mediated interactions

Lingfei Luo, Xiaoping Yang, Yoshihiro Takihara, Hendrik Knoetgen and Michael Kessel ()
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Lingfei Luo: Research Group Developmental Biology, Department of Molecular Cell Biology
Xiaoping Yang: Max Planck Institute for Biophysical Chemistry
Yoshihiro Takihara: Hiroshima University
Hendrik Knoetgen: Research Group Developmental Biology, Department of Molecular Cell Biology
Michael Kessel: Research Group Developmental Biology, Department of Molecular Cell Biology

Nature, 2004, vol. 427, issue 6976, 749-753

Abstract: Abstract Embryonic development is tightly controlled. The clustered genes of the Hox family of homeobox proteins play an important part in regulating this development and also proliferation. They specify embryonic structures along the body axis, and are associated with normal and malignant cell growth1,2,3,4. The cell-cycle regulator geminin controls replication by binding to the licensing factor Cdt1, and is involved in neural differentiation5,6,7. Here, we show that murine geminin associates transiently with members of the Hox-repressing polycomb complex, with the chromatin of Hox regulatory DNA elements and with Hox proteins. Gain- and loss-of-function experiments in the chick neural tube demonstrate that geminin modulates the anterior boundary of Hoxb9 transcription, which suggests a polycomb-like activity for geminin. The interaction between geminin and Hox proteins prevents Hox proteins from binding to DNA, inhibits Hox-dependent transcriptional activation of reporter and endogenous downstream target genes, and displaces Cdt1 from its complex with geminin. By establishing competitive regulation, geminin functions as a coordinator of developmental and proliferative control.

Date: 2004
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DOI: 10.1038/nature02305

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