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磷脂酰胆碱介导 LET-607 和 DAF-16 应激反应途径之间的串扰。

Phosphatidylcholine mediates the crosstalk between LET-607 and DAF-16 stress response pathways.

机构信息

School of Life Sciences, Chongqing University, Chongqing, China.

出版信息

PLoS Genet. 2021 May 20;17(5):e1009573. doi: 10.1371/journal.pgen.1009573. eCollection 2021 May.

DOI:10.1371/journal.pgen.1009573
PMID:34014977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8172019/
Abstract

Coordinated regulation of stress response pathways is crucial for cellular homeostasis. However, crosstalk between the different stress pathways and the physiological significance of this crosstalk remain poorly understood. In this study, using the model organism C. elegans, we discovered that suppression of the transcription factor LET-607/CREBH, a regulator of cellular defense and proteostatic responses, triggers adaptive induction of DAF-16-dependent stress responses. Suppression of LET-607 improves stress resistance and extends C. elegans lifespan in a DAF-16-dependent manner. We identified the sphingomyelin synthase SMS-5 to be a central mediator in the communication between LET-607 and DAF-16. SMS-5 reduces the contents of unsaturated phosphatidylcholine (PC), which activates DAF-16 through ITR-1-dependent calcium signaling and calcium-sensitive kinase PKC-2. Our data reveal the significance of crosstalk between different stress pathways in animal fitness and identify LET-607/CREBH and specific PC as regulators of DAF-16 and longevity.

摘要

协调应激反应途径的调控对于细胞内稳态至关重要。然而，不同应激途径之间的串扰及其生理意义仍知之甚少。在这项研究中，我们利用模式生物秀丽隐杆线虫发现，转录因子 LET-607/CREBH 的抑制，作为细胞防御和蛋白质稳态反应的调节剂，会触发 DAF-16 依赖性应激反应的适应性诱导。抑制 LET-607 以依赖于 DAF-16 的方式提高了线虫的应激抗性并延长了其寿命。我们确定了鞘磷脂合酶 SMS-5 是 LET-607 和 DAF-16 之间通讯的中心介质。SMS-5 降低了不饱和磷脂酰胆碱 (PC) 的含量，通过 ITR-1 依赖性钙信号和钙敏感激酶 PKC-2 激活 DAF-16。我们的数据揭示了不同应激途径之间串扰在动物适应性和生存能力中的重要性，并确定了 LET-607/CREBH 和特定的 PC 作为 DAF-16 和长寿的调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/4db56df314ae/pgen.1009573.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/0fadbac4fec9/pgen.1009573.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/176e49e3aff3/pgen.1009573.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/5bcc31fd375d/pgen.1009573.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/c9a1403b25c6/pgen.1009573.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/7d7b5e7e0442/pgen.1009573.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/4db56df314ae/pgen.1009573.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/0fadbac4fec9/pgen.1009573.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/be1f750ace50/pgen.1009573.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/e37f25cbad5e/pgen.1009573.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/176e49e3aff3/pgen.1009573.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/5bcc31fd375d/pgen.1009573.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/c9a1403b25c6/pgen.1009573.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/7d7b5e7e0442/pgen.1009573.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09e2/8172019/4db56df314ae/pgen.1009573.g008.jpg

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