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拟南芥 BIG 蛋白在肌醇稳态介导的细胞死亡中的作用。

Involvement of Arabidopsis BIG protein in cell death mediated by Myo-inositol homeostasis.

机构信息

Université Paris-Saclay, CNRS, INRAE, Univ Evry, Paris Diderot, Sorbonne Paris-Cité, Institute of Plant Sciences Paris-Saclay (IPS2), 91405, Orsay, France.

Institut Jean-Pierre Bourgin, INRAE, AgroParisTech, Université Paris-Saclay, 78000, Versailles, France.

出版信息

Sci Rep. 2020 Jul 9;10(1):11268. doi: 10.1038/s41598-020-68235-4.

DOI:10.1038/s41598-020-68235-4
PMID:32647331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7347573/
Abstract

Programmed cell death (PCD) is essential for several aspects of plant life. We previously identified the mips1 mutant of Arabidopsis thaliana, which is deficient for the enzyme catalysing myo-inositol synthesis, and that displays light-dependent formation of lesions on leaves due to Salicylic Acid (SA) over-accumulation. Rationale of this work was to identify novel regulators of plant PCD using a genetic approach. A screen for secondary mutations that abolish the mips1 PCD phenotype identified a mutation in the BIG gene, encoding a factor of unknown molecular function that was previously shown to play pleiotropic roles in plant development and defence. Physiological analyses showed that BIG is required for lesion formation in mips1 via SA-dependant signalling. big mutations partly rescued transcriptomic and metabolomics perturbations as stress-related phytohormones homeostasis. In addition, since loss of function of the ceramide synthase LOH2 was not able to abolish cell death induction in mips1, we show that PCD induction is not fully dependent of sphingolipid accumulation as previously suggested. Our results provide further insights into the role of the BIG protein in the control of MIPS1-dependent cell death and also into the impact of sphingolipid homeostasis in this pathway.

摘要

细胞程序性死亡(PCD)对于植物生命的几个方面至关重要。我们之前鉴定了拟南芥 mips1 突变体,该突变体缺乏催化肌醇合成的酶,并且由于水杨酸(SA)过度积累而表现出光依赖性叶片损伤。这项工作的原理是使用遗传方法鉴定植物 PCD 的新调节剂。筛选消除 mips1 PCD 表型的次级突变,鉴定了 BIG 基因的突变,该基因编码一种未知分子功能的因子,先前表明该因子在植物发育和防御中发挥多效作用。生理分析表明,BIG 通过 SA 依赖的信号传导对于 mips1 中的损伤形成是必需的。big 突变部分挽救了与胁迫相关的植物激素稳态相关的转录组和代谢组学扰动。此外,由于神经酰胺合酶 LOH2 的功能丧失不能消除 mips1 中的细胞死亡诱导,我们表明细胞程序性死亡的诱导并不完全依赖于先前提出的鞘脂积累。我们的研究结果为 BIG 蛋白在控制 MIPS1 依赖性细胞死亡中的作用以及鞘脂稳态在该途径中的影响提供了进一步的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/65ab751c0ddd/41598_2020_68235_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/f0ee4ad324f4/41598_2020_68235_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/7d45e09fe424/41598_2020_68235_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/c50dec3bab02/41598_2020_68235_Fig3a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/bd5cb9ebb4c0/41598_2020_68235_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/65ab751c0ddd/41598_2020_68235_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/f0ee4ad324f4/41598_2020_68235_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/7d45e09fe424/41598_2020_68235_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/c50dec3bab02/41598_2020_68235_Fig3a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/bd5cb9ebb4c0/41598_2020_68235_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7916/7347573/65ab751c0ddd/41598_2020_68235_Fig5_HTML.jpg

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