The TACPyAT repeats in the chalcone synthase promoter of Petunia hybrida act as a dominant negative cis-acting module in the control of organ-specific expression
Article first published online: 23 FEB 2005
The Plant Journal
Volume 2, Issue 4, pages 525–535, July 1992
How to Cite
van der Meer, I. M., Brouwer, M., Spelt, C. E., Mol, J.-N. M. and Stuitje, A. R. (1992), The TACPyAT repeats in the chalcone synthase promoter of Petunia hybrida act as a dominant negative cis-acting module in the control of organ-specific expression. The Plant Journal, 2: 525–535. doi: 10.1046/j.1365-313X.1992.t01-23-00999.x
- Issue published online: 23 FEB 2005
- Article first published online: 23 FEB 2005
- Received 25 June 1991 revised 18 February 1992
Analysis of the expression of the GUS reporter gene driven by various region of the Petunia hybrida chalcone synthase (chsA) promoter revealed that the developmental and organ-specific expression of the chsA gene is conferred by a TATA proximal module located between −67 and −53, previously designated as the TACPyAT repeats.
Histochemical analysis of GUS reporter gene expression revealed that the organ-specific 67 bp promoter fragment directs the same cell-type specificity as a 530 bp promoter, whereas additional enhancer sequences are present within the more TATA distal region. Moreover, the region between −800 and −530 is also involved in extending the cell-type specificity to the trichomes of flower organs and of young seedlings.
The mechanism by which the TACPyAT repeats modulate expression during plant development was studied by analysing the expression of the GUS gene driven by chimeric promoters consisting of the CaMV 35S enhancer(domain B, −750 to −90) fused to various chsA5′ upstream sequences. Detailed enzymatic and histochemical analysis revealed that in the presence of the TACPyAT module the CaMV 35S region only enhance GUS activity in those organs in which the chs A promoter is normally active. Furthermore, this analysis shows that enhancement in the presence of the CaMV 35S domain B is accomplished by increasing the number of cell types expressing the GUS gene within the organ, rather than enhancement of the chsA cell-type-specific expression within these organs. Deletion of the TACPyAT sequences in the chimeric promoter construct completely restores the well-documented CaMV 35S domain B cell-type specificity, showing that the TACPyAT module acts as a dominant negative cis-acting element which controls both organ and developmental regulation of the chsA promoter activity.