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Molecular and Cellular Biology, February 2004, p. 1058-1069, Vol. 24, No. 3
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.3.1058-1069.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Identification of MoKA, a Novel F-Box Protein That Modulates Krüppel-Like Transcription Factor 7 Activity

Silvia Smaldone, Friedrich Laub, Cindy Else, Cecilia Dragomir, and Francesco Ramirez*

Laboratory of Genetics and Organogenesis, Hospital for Special Surgery at the Weill Medical College of Cornell University, New York, New York 10021

Received 6 May 2003/ Returned for modification 16 June 2003/ Accepted 31 October 2003

KLF7, a member of the Krüppel-like transcription factor family, is believed to regulate neurogenesis and cell cycle progression. Here, a yeast two-hybrid screen for KLF7 cofactors in the developing nervous system identified a novel 140-kDa protein named MoKA, for modulator of KLF7 activity. Interaction between MoKA and KLF7 was confirmed by the in vitro glutathione S-transferase pull-down assay and by coimmunoprecipitation of the proteins overexpressed in mammalian cells. Functional assays documented that MoKA is a KLF7 coactivator, and in situ hybridizations identified the developing nervous system and the adult testes as two sites of MoKA and Klf7 coexpression. Chromatin immunoprecipitation experiments demonstrated KLF7 binding to the p21WAF1/Cip1 gene while transient transfection assays documented KLF7 stimulation of the p21WAF1/Cip1 proximal promoter. Additional tests revealed that distinct structural motifs of MoKA direct interaction with KLF7 and shuttling between the nucleus and cytoplasm of asynchronously cycling cells. Altogether, our results strongly suggest that MoKA and KLF7 interact functionally to regulate gene expression during cell differentiation and identify the cell cycle regulator p21WAF1/Cip1 as one of the targeted genes.

* Corresponding author. Mailing address: Laboratory of Genetics and Organogenesis, Hospital for Special Surgery at the Weill Medical College of Cornell University, 535 East 70th St., New York, NY 10021. Phone: (212) 774-7554. Fax: (212) 774-7864. E-mail: ramirezf{at}hss.edu.

Molecular and Cellular Biology, February 2004, p. 1058-1069, Vol. 24, No. 3
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.3.1058-1069.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Smaldone, S., Ramirez, F. (2006). Multiple pathways regulate intracellular shuttling of MoKA, a co-activator of transcription factor KLF7. Nucleic Acids Res 0: gkl659v3-9 [Abstract] [Full Text]  
  • Antoniv, T. T., Tanaka, S., Sudan, B., De Val, S., Liu, K., Wang, L., Wells, D. J., Bou-Gharios, G., Ramirez, F. (2005). Identification of a Repressor in the First Intron of the Human {alpha}2(I) Collagen Gene (COL1A2). J. Biol. Chem. 280: 35417-35423 [Abstract] [Full Text]  
  • Laub, F., Lei, L., Sumiyoshi, H., Kajimura, D., Dragomir, C., Smaldone, S., Puche, A. C., Petros, T. J., Mason, C., Parada, L. F., Ramirez, F. (2005). Transcription Factor KLF7 Is Important for Neuronal Morphogenesis in Selected Regions of the Nervous System. Mol. Cell. Biol. 25: 5699-5711 [Abstract] [Full Text]  


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