Light affects many physiological and developmental processes of plants by regulating the expression and activity of light responsive proteins. Among them, phytochrome interacting factors (PIFs) play pivotal roles in the regulation of anthocyanin accumulation and hypocotyl growth. However, the molecular mechanism is not well understood, especially in woody plants, such as apple (Malus × domestica). In this study, we identified a light responsive PIF protein, MdPIF7, in apple and investigated the molecular mechanism of its regulation of anthocyanin biosynthesis and hypocotyl growth. We found that overexpression of MdPIF7 decreased anthocyanin accumulation in transgenic apple materials and promoted hypocotyl elongation in ectopically expressed Arabidopsis (Arabidopsis thaliana). Further investigation showed that MdPIF7 functioned by interacting with B-box 23 (MdBBX23), a positive regulator of anthocyanin biosynthesis in apple and hypocotyl growth inhibition in ectopically expressed Arabidopsis, and attenuating the transcriptional activation of MdBBX23 on LONG HYPOCOTYL 5 (MdHY5). In addition, MdPIF7 interacted with basic region leucine zipper 44 (MdbZIP44) and ethylene response factor 38 (MdERF38), two positive regulators of anthocyanin biosynthesis, and it negatively regulated MdbZIP44- and MdERF38-promoted anthocyanin accumulation by interfering with the interaction between MdbZIP44/MdERF38 and MdMYB1. Taken together, our results reveal that MdPIF7 regulates anthocyanin biosynthesis in apple and hypocotyl growth in ectopically expressed Arabidopsis through MdPIF7-MdBBX23-MdHY5 and MdPIF7-MdbZIP44/MdERF38-MdMYB1 modules. Our findings enrich the functional studies of PIF proteins and provide insights into the molecular mechanism of PIF-mediated anthocyanin biosynthesis and hypocotyl growth.

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SUMMARYWounding stress leads to leaf senescence. However, the underlying molecular mechanism has not been elucidated. In this study, we investigated the role of the MdVQ10–MdWRKY75 module in wound‐induced leaf senescence. MdWRKY75 was identified as a key positive modulator of wound‐induced leaf senescence by activating the expression of the senescence‐associated genes MdSAG12 and MdSAG18. MdVQ10 interacted with MdWRKY75 to enhance MdWRKY75‐activated transcription of MdSAG12 and MdSAG18, thereby promoting leaf senescence triggered by wounding. In addition, the calmodulin‐like protein MdCML15 promoted MdVQ10‐mediated leaf senescence by stimulating the interaction between MdVQ10 and MdWRKY75. Moreover, the jasmonic acid signaling repressors MdJAZ12 and MdJAZ14 antagonized MdVQ10‐mediated leaf senescence by weakening the MdVQ10–MdWRKY75 interaction. Our results demonstrate that the MdVQ10–MdWRKY75 module is a key modulator of wound‐induced leaf senescence and provides insights into the mechanism of leaf senescence caused by wounding.