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. 2018 Jan 30;69(8):2061–2070. doi: 10.1093/jxb/ery028

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© The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Experimental Biology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 6. — Model of TF interactions in response to artificial high-CO₂ atmosphere (AHCA). AHCA treatment triggers the expression of various TFs, but only those with confirmed interactions are shown here. DkERF9, 10, and19 bind directly to, and activate promoters of, the anoxia-related genes DkADH1 and DkPDC2, which subsequently accelerate deastringency. DkERF18, 19, and DkMYB6, 10 physically bind and trans-activate DkERF promoters; DkERF21 and 22 are indirect regulators of DkERF10. DkERF19 exhibits auto-activation and binds to its own promoter. Solid arrows indicate direct interactions, while dashed arrows indicate indirect regulation.