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抑制拟南芥根愈伤组织中的组蛋白脱乙酰酶可促进芽器官发生。

Inhibition of histone deacetylase in Arabidopsis root calli promotes shoot organogenesis.

作者信息

Pan Qinwei, Huang Ruirui, Xiao Qiong, Wu Xuting, Jian Baoxia, Xiang Yanan, Gan Lijun, Liu Zongrang, Li Yi, Gu Tingting, Liu Huawei

机构信息

State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Horticulture, Nanjing Agricultural University, Nanjing, China.

Laboratory of Plant Hormone, College of Life Sciences, Nanjing Agricultural University, Nanjing, China.

出版信息

Front Plant Sci. 2025 Jan 27;15:1500573. doi: 10.3389/fpls.2024.1500573. eCollection 2024.

Abstract

organogenesis from somatic cells to the entire plant represents a remarkable biological phenomenon, but the underlying regulatory mechanism, particularly at the epigenetic level, remains obscure. In this work, we demonstrate the important role of histone deacetylases (HDACs) in shoot organogenesis. HDAC inhibition by trichostatin A (an HDAC inhibitor) at the callus induction stage promotes shoot formation in wounded roots and circumvents tissue wounding to initiate shoot regeneration in unwounded roots. This HDAC inhibition-mediated promotion of shoot organogenesis in wounded roots is associated with the concomitant upregulation of the wound signaling pathway (, etc.) and the ARF-LBD pathway (, etc.) and the downregulation of auxin biosynthesis and reduced auxin content. Furthermore, inhibiting HDACs enhances the local enrichment of histone 3 lysine 9/lysine 14 acetylation at , supporting the role of histone acetylation in its transcriptional regulation. On the other hand, the HDAC inhibition-associated activation of shoot organogenesis from unwounded roots is coupled with increased expression of the pathway gene while bypassing the wound signaling or auxin biosynthetic genes. These findings provide novel insights into the regulatory mechanisms underlying shoot organogenesis and lay a foundation for the improvement of plant transformation technologies.

摘要

从体细胞到整个植株的器官发生是一种显著的生物学现象,但其潜在的调控机制,尤其是表观遗传水平的调控机制,仍不清楚。在这项研究中,我们证明了组蛋白去乙酰化酶(HDACs)在芽器官发生中的重要作用。在愈伤组织诱导阶段,曲古抑菌素A(一种HDAC抑制剂)抑制HDAC可促进受伤根中芽的形成,并避免组织受伤以启动未受伤根中的芽再生。这种HDAC抑制介导的受伤根中芽器官发生的促进作用与伤口信号通路(如 等)和ARF-LBD通路(如 等)的同时上调以及生长素生物合成的下调和生长素含量的降低有关。此外,抑制HDACs可增强组蛋白3赖氨酸9/赖氨酸14乙酰化在 处的局部富集,支持组蛋白乙酰化在其转录调控中的作用。另一方面,HDAC抑制相关的未受伤根中芽器官发生的激活与 通路基因 的表达增加相关,同时绕过伤口信号或生长素生物合成基因。这些发现为芽器官发生的调控机制提供了新的见解,并为植物转化技术的改进奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dbd/11807735/8a4e98a07311/fpls-15-1500573-g001.jpg

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