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甾醇硫酸盐的自动抑制作用介导了形成赤潮的海洋硅藻的程序性细胞死亡。

Autoinhibitory sterol sulfates mediate programmed cell death in a bloom-forming marine diatom.

机构信息

Bio-Organic Chemistry Unit, CNR- Istituto di Chimica Biomolecolare (ICB) - CNR, Via Campi Flegrei 34, Pozzuoli, NA, 80078, Italy.

出版信息

Nat Commun. 2017 Nov 3;8(1):1292. doi: 10.1038/s41467-017-01300-1.

Abstract

Cell mortality is a key mechanism that shapes phytoplankton blooms and species dynamics in aquatic environments. Here we show that sterol sulfates (StS) are regulatory molecules of a cell death program in Skeletonema marinoi, a marine diatom-blooming species in temperate coastal waters. The molecules trigger an oxidative burst and production of nitric oxide in a dose-dependent manner. The intracellular level of StS increases with cell ageing and ultimately leads to a mechanism of apoptosis-like death. Disrupting StS biosynthesis by inhibition of the sulfonation step significantly delays the onset of this fatal process and maintains steady growth in algal cells for several days. The autoinhibitory activity of StS demonstrates the functional significance of small metabolites in diatoms. The StS pathway provides another view on cell regulation during bloom dynamics in marine habitats and opens new opportunities for the biochemical control of mass-cultivation of microalgae.

摘要

细胞死亡是塑造水生环境中浮游植物爆发和物种动态的关键机制。在这里,我们表明甾醇硫酸盐 (StS) 是海洋硅藻爆发物种——海洋硅藻 Skeletonema marinoi 中细胞死亡程序的调节分子。这些分子以剂量依赖的方式触发氧化爆发和一氧化氮的产生。StS 的细胞内水平随着细胞老化而增加,最终导致类似细胞凋亡的死亡机制。通过抑制磺化步骤来破坏 StS 的生物合成会显著延迟这一致命过程的发生,并使藻类细胞在几天内保持稳定的生长。StS 的自动抑制活性证明了小代谢物在硅藻中的功能意义。StS 途径为海洋生境中爆发动态期间的细胞调控提供了另一种视角,并为大规模培养微藻的生化控制开辟了新的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b0f/5670183/96a1a82e60f9/41467_2017_1300_Fig1_HTML.jpg

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