MdNAC4 Interacts With MdAPRR2 to Regulate Nitrogen Deficiency-Induced Leaf Senescence in Apple (Malus domestica)

• Published in: Frontiers in plant science 2022-06, Vol.13, p.925035-925035
• Main Authors: Wen, Binbin, Gong, Xingyao, Tan, Qiuping, Zhao, Wenzhe, Chen, Xiude, Li, Dongmei, Li, Ling, Xiao, Wei
• Format: Article
• Language: English
• Subjects: apple; leaf senescence; MdAPRR2; MdNAC4; N deficiency; Plant Science
• ISSN: 1664-462X; 1664-462X
• DOI: 10.3389/fpls.2022.925035

Nitrogen (N) is one of the important macronutrients in plants, and N deficiency induces leaf senescence. However, the molecular mechanism underlying how N deficiency affects leaf senescence is unclear. Here, we report an apple NAC TF, MdNAC4, that participates in N deficiency-induced leaf senescence. The senescence phenotype of apple leaves overexpressing MdNAC4 was enhanced after N deficiency. Consistently, the chlorophyll content of transgenic leaves was significantly lower than that in the WT control leaves, the expression of chlorophyll catabolism-related genes ( MdNYC1 , MdPAO , and MdSGR1 ) was significantly higher than that in the WT controls, and the expression of chlorophyll synthesis-related genes ( MdHEMA , MdCHLI , and MdCHLM ) was significantly lower than that in the WT control leaves. Furthermore, MdNAC4 was found to directly activate the transcription of the chlorophyll catabolism-related genes MdNYC1 and MdPAO . Additionally, MdNAC4 was proven to interact with MdAPRR2 proteins both in vitro and in vivo , and overexpression of MdAPRR2 seemed to delay N deficiency-induced leaf senescence. Correspondingly, the chlorophyll loss of MdAPRR2-overexpressing (MdAPRR2-OE) lines was significantly lower than in WT control plants. Although downregulated, the expression of the chlorophyll synthesis-related genes MdHEMA , MdCHLI , and MdCHLM in the transgenic plants was more than twice that in the WT control plants. Taken together, our results enrich the regulatory network of leaf senescence induced by N deficiency through the interaction between MdNAC4 and MdAPRR2.