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. 2023 Aug 30;75(6):1741–1753. doi: 10.1093/jxb/erad341

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© The Author(s) 2023. 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 (https://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. 2. — A model of JA- and topping-dependent induction of nicotine biosynthesis genes in tobacco. ERF199 and ERF189 up-regulate nicotine biosynthesis genes (e.g. QPT2) by recognizing GC-rich elements in their promoter regions. A bHLH-family MYC2 transcription factor mediates JA-dependent induction of ERF genes. MYC2 is a direct target of JAZ repressors. When a co-complex comprising COI1 and JAZ perceives a JA signal, JAZ proteins are removed through proteasome-dependent degradation. MYC2 also directly up-regulates nicotine biosynthesis genes by recognizing G-box elements as homo- and/or heterodimers. Topping induces nta-TMX27 expression, leading to nta-miRX27 degradation. Degradation of this miRNA relieves its inhibition of QPT2, resulting in enhanced QPT2 expression.