ScRNA‐seq reveals dark‐ and light‐induced differentially expressed gene atlases of seedling leaves in Arachis hypogaea L.

花生 生物 拟南芥 黄化 基因 植物 细胞生物学 细胞分裂 转录组 形态发生 转录因子 细胞周期 基因表达 基因表达谱 细胞 遗传学 突变体 生物化学
作者
Quanqing Deng,Puxuan Du,Sunil S. Gangurde,Yanbin Hong,Yuan Xiao,Dongxiu Hu,Haifen Li,Qing Lu,Shaoxiong Li,Haiyan Liu,Runfeng Wang,Lu Huang,Wenyi Wang,Vanika Garg,Xuanqiang Liang,Rajeev K. Varshney,Xiaoping Chen,Hao Liu
出处
期刊:Plant Biotechnology Journal [Wiley]
卷期号:22 (7): 1848-1866 被引量:8
标识
DOI:10.1111/pbi.14306
摘要

Summary Although the regulatory mechanisms of dark and light‐induced plant morphogenesis have been broadly investigated, the biological process in peanuts has not been systematically explored on single‐cell resolution. Herein, 10 cell clusters were characterized using scRNA‐seq‐identified marker genes, based on 13 409 and 11 296 single cells from 1‐week‐old peanut seedling leaves grown under dark and light conditions. 6104 genes and 50 transcription factors (TFs) displayed significant expression patterns in distinct cell clusters, which provided gene resources for profiling dark/light‐induced candidate genes. Further pseudo‐time trajectory and cell cycle evidence supported that dark repressed the cell division and perturbed normal cell cycle, especially the PORA abundances correlated with 11 TFs highly enriched in mesophyll to restrict the chlorophyllide synthesis. Additionally, light repressed the epidermis cell developmental trajectory extending by inhibiting the growth hormone pathway, and 21 TFs probably contributed to the different genes transcriptional dynamic. Eventually, peanut AHL17 was identified from the profile of differentially expressed TFs, which encoded protein located in the nucleus promoted leaf epidermal cell enlargement when ectopically overexpressed in Arabidopsis through the regulatory phytohormone pathway. Overall, our study presents the different gene atlases in peanut etiolated and green seedlings, providing novel biological insights to elucidate light‐induced leaf cell development at the single‐cell level.
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