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营养感知的细胞周期。

Nutrition-minded cell cycle.

机构信息

Department of Microbiology, University of California, Davis, CA 95616, USA.

出版信息

Sci Signal. 2009 Nov 10;2(96):pe74. doi: 10.1126/scisignal.296pe74.

DOI:10.1126/scisignal.296pe74
PMID:19903940
Abstract

For decades, the fission yeast Schizosaccharomyces pombe has been used as an excellent model with which to explore how cellular growth is coordinated with the division cycle, a yet-unanswered question in biology. New studies in this organism show that TOR (target of rapamycin) kinase and stress-responsive MAPK (mitogen-activated protein kinase) form a signaling pathway that readjusts the timing of mitotic onset in response to poor nutrient conditions. Nutritional environment appears to be translated into graded activity of the protein kinases that influence the activation of Cdc2, a cyclin-dependent kinase driving cell-cycle progression.

摘要

几十年来,裂殖酵母 Schizosaccharomyces pombe 一直被用作探索细胞生长如何与分裂周期相协调的优秀模型,这是生物学中一个尚未解决的问题。该生物的新研究表明,TOR(雷帕霉素靶蛋白)激酶和应激反应性 MAPK(丝裂原活化蛋白激酶)形成了一个信号通路,根据营养条件的变化来重新调整有丝分裂起始的时间。营养环境似乎被转化为影响细胞周期进程的 cyclin-dependent kinase Cdc2 激活的蛋白激酶的分级活性。

相似文献

1
Nutrition-minded cell cycle.营养感知的细胞周期。
Sci Signal. 2009 Nov 10;2(96):pe74. doi: 10.1126/scisignal.296pe74.
2
TOR signalling regulates mitotic commitment through stress-activated MAPK and Polo kinase in response to nutrient stress.TOR信号通路通过应激激活的丝裂原活化蛋白激酶(MAPK)和波罗蛋白激酶,在营养应激反应中调节有丝分裂承诺。
Biochem Soc Trans. 2009 Feb;37(Pt 1):273-7. doi: 10.1042/BST0370273.
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TOR signalling regulates mitotic commitment through the stress MAP kinase pathway and the Polo and Cdc2 kinases.TOR信号传导通过应激丝裂原活化蛋白激酶途径以及Polo激酶和Cdc2激酶来调节有丝分裂的启动。
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Mcs4 mitotic catastrophe suppressor regulates the fission yeast cell cycle through the Wik1-Wis1-Spc1 kinase cascade.Mcs4有丝分裂灾难抑制因子通过Wik1-Wis1-Spc1激酶级联反应调节裂殖酵母细胞周期。
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Quantitative Phosphoproteomics Reveals the Signaling Dynamics of Cell-Cycle Kinases in the Fission Yeast Schizosaccharomyces pombe.定量磷酸化蛋白质组学揭示了裂殖酵母 Schizosaccharomyces pombe 细胞周期激酶的信号动态。
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Fission yeast Tor1 functions as part of TORC1 to control mitotic entry through the stress MAPK pathway following nutrient stress.裂殖酵母Tor1作为TORC1的一部分发挥作用,在营养应激后通过应激丝裂原活化蛋白激酶(MAPK)途径控制有丝分裂进入。
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Polo kinase links the stress pathway to cell cycle control and tip growth in fission yeast.Polo激酶将应激途径与裂殖酵母中的细胞周期控制和顶端生长联系起来。
Nature. 2005 May 26;435(7041):507-12. doi: 10.1038/nature03590.
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The spindle pole body plays a key role in controlling mitotic commitment in the fission yeast Schizosaccharomyces pombe.纺锤极体在裂殖酵母粟酒裂殖酵母中控制有丝分裂起始过程中起着关键作用。
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Activity of Cdc2 and its interaction with the cyclin Cdc13 depend on the molecular chaperone Cdc37 in Schizosaccharomyces pombe.在粟酒裂殖酵母中,Cdc2的活性及其与细胞周期蛋白Cdc13的相互作用依赖于分子伴侣Cdc37。
J Cell Sci. 2006 Jan 15;119(Pt 2):292-302. doi: 10.1242/jcs.02729. Epub 2006 Jan 3.
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Fission yeast TOR complex 2 activates the AGC-family Gad8 kinase essential for stress resistance and cell cycle control.裂殖酵母TOR复合体2激活AGC家族的Gad8激酶,该激酶对压力抗性和细胞周期控制至关重要。
Cell Cycle. 2008 Feb 1;7(3):358-64. doi: 10.4161/cc.7.3.5245. Epub 2007 Nov 1.

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Curr Genet. 2021 Aug;67(4):519-534. doi: 10.1007/s00294-021-01177-0. Epub 2021 Mar 29.
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Nuclear Functions of TOR: Impact on Transcription and the Epigenome.TOR 的核功能:对转录和表观基因组的影响。
Genes (Basel). 2020 Jun 10;11(6):641. doi: 10.3390/genes11060641.
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Stable Pom1 clusters form a glucose-modulated concentration gradient that regulates mitotic entry.
稳定的 Pom1 簇形成一个葡萄糖调节的浓度梯度,调节有丝分裂的进入。
Elife. 2019 May 3;8:e46003. doi: 10.7554/eLife.46003.
4
SakA and MpkC Stress MAPKs Show Opposite and Common Functions During Stress Responses and Development in .在应激反应和发育过程中,SakA和MpkC应激丝裂原活化蛋白激酶表现出相反和共同的功能。 (注:原文句末不完整,缺少具体对象,我根据常见语境补充了“在……中”,使译文更通顺。)
Front Microbiol. 2018 Oct 23;9:2518. doi: 10.3389/fmicb.2018.02518. eCollection 2018.
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S-Adenosylmethionine Synthetase Is Required for Cell Growth, Maintenance of G0 Phase, and Termination of Quiescence in Fission Yeast.S-腺苷甲硫氨酸合成酶是裂殖酵母细胞生长、维持G0期以及静止期终止所必需的。
iScience. 2018 Jul 27;5:38-51. doi: 10.1016/j.isci.2018.06.011. Epub 2018 Jun 30.
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Glucose restriction induces transient G2 cell cycle arrest extending cellular chronological lifespan.葡萄糖限制诱导短暂的G2期细胞周期停滞,从而延长细胞的时序寿命。
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PKA antagonizes CLASP-dependent microtubule stabilization to re-localize Pom1 and buffer cell size upon glucose limitation.蛋白激酶A(PKA)拮抗CLASP依赖的微管稳定作用,以便在葡萄糖受限的情况下重新定位Pom1并缓冲细胞大小。
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