Abstract
The members of the GATA family of transcription factors have homologous zinc fingers and bind to similar sequence motifs. Recent advances in genome-wide technologies and the integration of bioinformatics data have led to a better understanding of how GATA factors regulate gene expression; GATA-factor-induced transcriptional and epigenetic changes have now been analyzed at unprecedented levels of detail. Here, we review the results of genome-wide studies of GATA factor occupancy in human and murine cell lines and primary cells (as determined by chromatin immunoprecipitation sequencing), and then discuss the molecular mechanisms underlying the mediation of transcriptional and epigenetic regulation by GATA factors.
Highlights
The GATA family of transcription factors comprises six members (GATA1–GATA6) that are expressed in various cell types and are involved in numerous physiologic and pathologic processes
The analysis of GATA3 ChIP-seq profiles at different stages of T cell development showed that GATA3 genome-wide occupancy is cell-specific: distinct sets of GATA3-bound genes were identified at each stage in T cell development, whereas only a few binding sites were conserved among the various T cell types; these findings suggest that in each cell context, distinct co-factors may have critical roles in the differential binding of GATA3.101 By the way of example, the genomic distribution of GATA3 binding profiles differs in human Th1 versus T helper 2 (Th2) cells, and GATA3 distribution in Th1 cells is mediated by T-bet
ChIP-seq analyses of the ETS factor FLI1 in Th2 cells and RUNX1 in T cell acute lymphoid leukemia (T-ALL) cell lines showed that both factors colocalize with GATA3.101,108 These findings suggest that GATA3 cooperates with FLI1 and RUNX1 to regulate the transcription of its target genes
Summary
The GATA family of transcription factors comprises six members (GATA1–GATA6) that are expressed in various cell types and are involved in numerous physiologic and pathologic processes.
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