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Figure 1 | BMC Molecular Biology

Figure 1

From: GATA elements control repression of cardiac troponin I promoter activity in skeletal muscle cells

Figure 1

The cTnI promoter is activated by mutation or deletion of GATA sites in skeletal muscle in vivo. Transfection experiments of cTnI-CAT constructs in regenerating rat soleus muscles. The -230/+16 cTnI promoter and different mutants are schematically represented on the left, the three GATA site being indicated with squares and the A/T rich element with an oval. CAT activities in transfected muscles are shown on the right. The following mutants were examined (top to bottom): -145 and -127 deletion mutants, leading to the deletion of two of three or all three GA-rich sequences, respectively; mutation of the A/T-rich sequence (filled oval); GATA → CACA mutation of the proximal GATA site (crossed square); GATA → CACA mutation of the two distal GATA sites (two crossed squares); GATA → CACA mutation of all three GATA sites (three crossed squares); deletion of the two distal GATA sites; GATA → GCCA mutation of all three GATA sites (filled squares). Note that deletion/mutation of GATA sites leads to increased activity of the cTnI promoter, up to levels even higher than the SV40 promoter. Values (means ± S.E.) are expressed as fold increase in CAT activity over the promoterless construct. Each construct was tested in 4 to 8 independent experiments.

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