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PLoS One. 2012;7(11):e50637. doi: 10.1371/journal.pone.0050637. Epub 2012 Nov 30.

SUMOylation regulates the transcriptional repression activity of FOG-2 and its association with GATA-4.

Author information

  • 1Department of Medicine, St George Clinical School, University of New South Wales, Sydney, New South Wales, Australia. j.perdomo@unsw.edu.au

Erratum in

  • PLoS One. 2013;8(5). doi:10.1371/annotation/3d7a31cd-09e7-47d1-af57-c58c7082058d.

Abstract

Friend of GATA 2 (FOG-2), a co-factor of several GATA transcription factors (GATA-4, -5 and 6), is a critical regulator of coronary vessel formation and heart morphogenesis. Here we demonstrate that FOG-2 is SUMOylated and that this modification modulates its transcriptional activity. FOG-2 SUMOylation occurs at four lysine residues (K324, 471, 915, 955) [corrected]. Three of these residues are part of the characteristic SUMO consensus site (ψKXE), while K955 is found in the less frequent TKXE motif. Absence of SUMOylation did not affect FOG-2's nuclear localization. However, mutation of the FOG-2 SUMOylation sites, or de-SUMOylation, with SENP-1 or SENP-8 resulted in stronger transcriptional repression activity in both heterologous cells and cardiomyocytes. Conversely, increased FOG-2 SUMOylation by overexpression of SUMO-1 or expression of a SUMO-1-FOG-2 fusion protein rendered FOG-2 incapable of repressing GATA-4-mediated activation of the B-type natriuretic peptide (BNP) promoter. Moreover, we demonstrate both increased interaction between a FOG-2 SUMO mutant and GATA-4 and enhanced SUMOylation of wild-type FOG-2 by co-expression of GATA-4. These data suggest a new dynamics in which GATA-4 may alter the activity of FOG-2 by influencing its SUMOylation status.

PMID:
23226341
[PubMed - indexed for MEDLINE]
PMCID:
PMC3511347
Free PMC Article
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