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A more recent version of this article appeared on September 1, 2000
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Papers In Press, published online ahead of print June 21, 2000
J. Biol. Chem, 10.1074/jbc.M000020200
Submitted on January 3, 2000
Revised on June 14, 2000
Accepted on June 20, 2000

GATA Zinc Finger Interactions Modulate DNA Binding and Transactivation

Cecelia D. Trainor, Rodolfo Ghirlando, and Melanie A. Simpson

LMB, NIDDK, NIH, Bethesda, MD 20892

Corresponding Author: ceceliat{at}intra.niddk.nih.gov

GATA-1 and other vertebrate GATA factors contain a DNA binding domain composed of two adjacent homologous zinc fingers. Whereas only the C-terminal finger of GATA-1 is capable of independent binding to the GATA recognition sequence, double GATA sites which require both fingers for high affinity interaction are found in several genes. We propose a mechanism whereby adjacent zinc fingers interact to influence the binding and transactivation properties of GATA-1 at a subset of DNA binding sites. Using two such double GATA sites we demonstrate that the N-terminal finger and adjacent linker region can alter the binding specificity of the C-terminal finger sufficiently to prevent it from recognizing some consensus GATA sequences. Therefore, the two zinc fingers form a composite binding domain having a different DNA-binding specificity from that shown by the constituent single C-terminal finger. Furthermore, we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation, namely, the sequence of the DNA binding site can alter the ability of GATA-1 to stimulate transcription.


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