Wei Ming, Zhang Mengqiu, Sun Jiali, Zhao Ying, Pak Solme, Ma Miaomiao, Chen Yingxi, Lu Han, Yang Jingli, Wei Hairong, Li Yuhua, Li Chenghao
State Key Laboratory of Tree Genetics and Breeding, School of Forestry, Northeast Forestry University, Harbin, 150040, China.
College of Life Sciences, Northeast Forestry University, Harbin, 150040, China.
J Integr Plant Biol. 2023 Mar;65(3):791-809. doi: 10.1111/jipb.13389. Epub 2022 Dec 31.
It is of great importance to better understand how trees regulate nitrogen (N) uptake under N deficiency conditions which severely challenge afforestation practices, yet the underlying molecular mechanisms have not been well elucidated. Here, we functionally characterized PuHox52, a Populus ussuriensis HD-ZIP transcription factor, whose overexpression greatly enhanced nutrient uptake and plant growth under N deficiency. We first conducted an RNA sequencing experiment to obtain root transcriptome using PuHox52-overexpression lines of P. ussuriensis under low N treatment. We then performed multiple genetic and phenotypic analyses to identify key target genes of PuHox52 and validated how they acted against N deficiency under PuHox52 regulation. PuHox52 was specifically induced in roots by N deficiency, and overexpression of PuHox52 promoted N uptake, plant growth, and root development. We demonstrated that several nitrate-responsive genes (PuNRT1.1, PuNRT2.4, PuCLC-b, PuNIA2, PuNIR1, and PuNLP1), phosphate-responsive genes (PuPHL1A and PuPHL1B), and an iron transporter gene (PuIRT1) were substantiated to be direct targets of PuHox52. Among them, PuNRT1.1, PuPHL1A/B, and PuIRT1 were upregulated to relatively higher levels during PuHox52-mediated responses against N deficiency in PuHox52-overexpression lines compared to WT. Our study revealed a novel regulatory mechanism underlying root adaption to N deficiency where PuHox52 modulated a coordinated uptake of nitrate, phosphate, and iron through 'PuHox52-PuNRT1.1', 'PuHox52-PuPHL1A/PuPHL1B', and 'PuHox52-PuIRT1' regulatory relationships in poplar roots.
深入了解树木在氮素缺乏条件下如何调节氮素吸收至关重要,因为氮素缺乏严重挑战造林实践,但其潜在的分子机制尚未得到充分阐明。在此,我们对大青杨HD-ZIP转录因子PuHox52进行了功能表征,其过表达在氮素缺乏条件下极大地增强了养分吸收和植物生长。我们首先进行了RNA测序实验,以获取低氮处理下大青杨PuHox52过表达株系的根系转录组。然后,我们进行了多项遗传和表型分析,以鉴定PuHox52的关键靶基因,并验证它们在PuHox52调控下如何应对氮素缺乏。氮素缺乏特异性诱导PuHox52在根中表达,PuHox52的过表达促进了氮素吸收、植物生长和根系发育。我们证明,几个硝酸盐响应基因(PuNRT1.1、PuNRT2.4、PuCLC-b、PuNIA2、PuNIR1和PuNLP1)、磷酸盐响应基因(PuPHL1A和PuPHL1B)以及一个铁转运基因(PuIRT1)被证实是PuHox52的直接靶标。其中,与野生型相比,在PuHox52过表达株系中,PuHox52介导的对氮素缺乏的响应过程中,PuNRT1.1、PuPHL1A/B和PuIRT1上调至相对较高水平。我们的研究揭示了根系适应氮素缺乏的一种新的调控机制,其中PuHox52通过杨树根中的“PuHox52-PuNRT1.1”、“PuHox52-PuPHL1A/PuPHL1B”和“PuHox52-PuIRT1”调控关系调节硝酸盐、磷酸盐和铁的协同吸收。