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Sulfur sequestration promotes multicellularity during nutrient limitation

机译：硫封存在营养限制期间促进多细胞性

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摘要

The behaviour of Dictyostelium discoideum depends on nutrients(1). When sufficient food is present these amoebae exist in a unicellular state, but upon starvation they aggregate into a multicellular organism(2,3). This biology makes D. discoideum an ideal model for investigating how fundamental metabolism commands cell differentiation and function. Here we show that reactive oxygen species-generated as a consequence of nutrient limitation-lead to the sequestration of cysteine in the antioxidant glutathione. This sequestration limits the use of the sulfur atom of cysteine in processes that contribute to mitochondrial metabolism and cellular proliferation, such as protein translation and the activity of enzymes that contain an iron-sulfur cluster. The regulated sequestration of sulfur maintains D. discoideum in a nonproliferating state that paves the way for multicellular development. This mechanism of signalling through reactive oxygen species highlights oxygen and sulfur as simple signalling molecules that dictate cell fate in an early eukaryote, with implications for responses to nutrient fluctuations in multicellular eukaryotes.
机译：dictyostelium discoideum的行为取决于营养素（1）。当存在足够的食物时，这些amoebae存在于单细胞状态下，但在饥饿后它们聚集成多细胞生物（2,3）。该生物学使D. Discoideum成为研究基本新陈代谢指挥细胞分化和功能的理想模型。在这里，我们表明，由于营养率限制导致的活性氧物种 - 导致抗氧化酸谷胱甘肽中的半胱氨酸的螯合。该隔离限制了半胱氨酸中的硫原子在有助于线粒体代谢和细胞增殖的方法中，例如蛋白翻译和含有铁硫簇的酶活性。硫的调节螯合在铺平多细胞发育方式的不溶解状态下保持D. DiveoIDEUM。通过反应性氧物质的这种信号机理突出了​​氧气和硫作为在早期真核生物中规定细胞命运的简单信号传导分子，其意义用于对多细胞真核生物中的营养波动进行反应。

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  • 来源
    《Nature》 |2021年第7850期|471-476|共6页
  • 作者

    Kelly Beth; Carrizo Gustavo E.; Edwards-Hicks Joy; Sanin David E.; Stanczak Michal A.; Priesnitz Chantal; Flachsmann Lea J.; Curtis Jonathan D.; Mittler Gerhard; Musa Yaarub; Becker Thomas; Buescher Joerg M.; Pearce Erika L.;

  • 作者单位

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Univ Freiburg Fac Med Inst Biochem & Mol Biol ZMBZ Freiburg Germany|Univ Freiburg Fac Biol Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Univ Bonn Fac Med Inst Biochem & Mol Biol Bonn Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany;

    Max Planck Inst Immunobiol & Epigenet Freiburg Germany|Johns Hopkins Univ Bloomberg Kimmel Inst Canc Immunotherapy Johns Ho Baltimore MD 21218 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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