GATA transcription factors

GATA transcription factors are representative of factors controlling cell differentiation. GATA-1 controls haematopoietic stem cells, GATA-3 is involved in the control of differentiation of thymocytes, and GATA-4 is a heart-specific transcription factor which has been implicated in the activation of genes responsible for cardiac hypertrophy. 

Fig. 1. Result of oligo-analysis on the upstream sequences of the 27 genes responding to nitrogen depletion. The first discovered pattern corresponds to the binding site of the GATA transcription factors and the second one to GCN4.

HEiCKLEN-KLEiN A, MCREYNOLDS LJ, EVANS T (2005), Using the zebrafish model to study GATA transcription factors , Semin. Cell Dev Biol, 16,95-106. 

NFAT2 plays a key role in the development of the embryo s heart. In the precursor cells, there is a temporal and spatial specific expression of NFAT2, which directs the formation of the valves and the septum in the heart. In the adult heart, NFAT proteins also cooperate with transcription factors of the GATA and MEF2 families to regulate cardiac muscle hypertrophic responses. 

Roy S, Cain KJ, Chapin RB, Charboneau RG, Barke RA (1998) Morphine modulates NF kappa B activation in macrophages. Biochem Biophys Res Commun 245 392-396 Roy S, Wang J, Gupta S, Charboneau R, Loh HH, Barke RA (2004) Chronic morphine treatment differentiates T helper cells to Th2 effector cells by modulating transcription factors GATA 3 and T-bet. J Neuroimmunol 147 78-81... 

Further covalent modifications of regulatory DNA-binding proteins include acetylation (e.g. of Lys residues in the transcription factor GATA-1 (Boyes et al., 1998)) and ADP-ribosylation (see 5.5.2), to name a few. 

Most of the control of tissue-specific gene expression occurs at the level of transcription this is achieved with tissue-specific transcription factors. For example, all genes that are to be expressed in erythroid cells, e.g., globin, spectrin, and erythropoietin receptor, have the site -AGATA- in their promoters. This site binds to a transcription factor (called GATA-l) which is present only in erythroid cells, and the promoter will function only in the presence of this factor. 

Cell-specific regulation is carried out in cooperation with a common transcriptional activator, the CREB-binding protein (CBP) (see above) which cooperates with the cell-specific transcriptional activator, FOG (friend of GATA-1), and controls the activity of the transcription factor, GATA-1. 

NF-AT3 also cooperates with GATA-4, a heart-specific transcription factor. When Ca2+ levels rise in a stressed heart, NF-AT3 moves to the nucleus and binds to GATA-4 and both turn on genes responsible for cardiac hypertrophy. The clinical importance of cardiac hypertrophy, which eventually causes heart failure, makes the development of drugs that act like immunosuppressives, preventing nuclear import of NF-AT3, an active area of research into control of cardiac hypertrophy. ... 

Boyes J, et al. Regulation of activity of the transcription factor GATA-1 by acetylation. Nature 1998 396 594-598. 

Gaedigk et al. (20) have demonstrated that there is tissue-specific expression of microsomal HYLl and not a single HYLl transcript and promoter region. Liang et al. (23) identified several potential cis-regulatory elements and found that transcription factor GATA-4 is probably the principal factor regulating liver specific expression. 

McDevitt MA, Shivdasani RA, Fujiwara Y, et al. A "knockdown" mutation created by cis-element gene targeting reveals the dependence of erythroid cell maturation on the level of transcription factor GATA-1. Proc Natl Acad Sci USA. 1997 94 6781-6785. 

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