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Molecular and Cellular Biology, October 1999, p. 7001-7010, Vol. 19, No. 10
Department of Physiology and Biophysics,
University of Iowa, Iowa City, Iowa 52242
Received 21 August 1998/Returned for modification 2 February
1999/Accepted 26 July 1999
Pitx2 is a newly described bicoid-like homeodomain transcription
factor that is defective in Rieger syndrome and shows a striking leftward developmental asymmetry. We have previously shown that Pitx2
(also called Ptx2 and RIEG) transactivates a reporter gene containing a
bicoid enhancer and synergistically transactivates the
prolactin promoter in the presence of the POU homeodomain protein
Pit-1. In this report, we focused on the C-terminal region which is
mutated in some Rieger patients and contains a highly conserved
14-amino-acid element. Deletion analysis of Pitx2 revealed that the
C-terminal 39-amino-acid tail represses DNA binding activity and is
required for Pitx2-Pit-1 interaction and Pit-1 synergism. Pit-1
interaction with the Pitx2 C terminus masks the inhibitory effect and
promotes increased DNA binding activity. Interestingly, cotransfection
of an expression vector encoding the C-terminal 39 amino acids of Pitx2
specifically inhibits Pitx2 transactivation activity. In contrast, the
C-terminal 39-amino-acid peptide interacts with Pitx2 to increase its
DNA binding activity. These data suggest that the C-terminal tail
intrinsically inhibits the Pitx2 protein and that this inhibition can
be overcome by interaction with other transcription factors to allow
activation during development.
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Multifunctional Role of the Pitx2 Homeodomain
Protein C-Terminal Tail
*
Corresponding author. Present address: Department of
Biological Science, The University of Tulsa, 600 S. College Ave.,
Tulsa, OK 74104-3189. Phone: (918) 631-2204. Fax: (918) 631-2762. E-mail: brad-amendt{at}utulsa.edu.
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