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. 2021 Oct 13;1:12. doi: 10.1186/s43897-021-00017-6

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Physical interaction of AtNAP with the AtCKX3 promoter revealed by yeast one-hybrid assay. (A) Schematic representation of the constructs in the studies. The expression of prey GAD fused with or without (negative control or Ctr) AtNAP were driven by the GAL1 promoter (P_GAL1). The LacZ gene driven by AtCKX3 promoter or its truncations or mutations served as the bait. (B) Activation of the LacZ reporter by binding of the fusion protein GAD-AtNAP to the AtCKX3 promoter. The AtCKX1 promoter lacked the motif and served as the other control. Blue color suggests a binding. The sequence in red represents the motif which AtNAP binds to. A of the translation start site was numbered as + 1. (C) Failure of AtNAP binding to the AtCKX3 promoter either containing transversion mutation or deletion of the motif sequence