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脂质生物合成及其与细胞周期进程的协调。

Lipid biosynthesis and its coordination with cell cycle progression.

作者信息

Kwok Alvin C M, Wong Joseph T Y

机构信息

Department of Biology, Hong Kong University of Science and Technology, Clearwater Bay, Kowloon, Hong Kong SAR, PR China.

出版信息

Plant Cell Physiol. 2005 Dec;46(12):1973-86. doi: 10.1093/pcp/pci213. Epub 2005 Oct 20.

Abstract

The activation of cell cycle regulators at the G1/S boundary has been linked to the cellular protein synthesis rate. It is conceivable that regulatory mechanisms are required to allow cells to coordinate the synthesis of other macromolecules with cell cycle progression. The availability of highly synchronized cells and flow cytometric methods facilitates investigation of the dynamics of lipid synthesis in the entire cell cycle of the heterotrophic dinoflagellate Crypthecodinium cohnii. Flow cytograms of Nile red-stained cells revealed a stepwise increase in the polar lipid content and a continuous increase in neutral lipid content in the dinoflagellate cell cycle. A cell cycle delay at early G1, but not G2/M, was observed upon inhibition of lipid synthesis. However, lipid synthesis continued during cell cycle arrest at the G1/S transition. A cell cycle delay was not observed when inhibitors of cellulose synthesis and fatty acid synthesis were added after the late G1 phase of the cell cycle. This implicates a commitment point that monitors the synthesis of fatty acids at the late G1 phase of the dinoflagellate cell cycle. Reduction of the glucose concentration in the medium down-regulated the G1 cell size with a concomitant forward shift of the commitment point. Inhibition of lipid synthesis up-regulated cellulose synthesis and resulted in an increase in cellulosic contents, while an inhibition of cellulose synthesis had no effects on lipid synthesis. Fatty acid synthesis and cellulose synthesis are apparently coupled to the cell cycle via independent pathways.

摘要

细胞周期调节因子在G1/S边界的激活与细胞蛋白质合成速率有关。可以想象,需要调节机制来使细胞协调其他大分子的合成与细胞周期进程。高度同步化的细胞和流式细胞术方法的可用性有助于研究异养甲藻隐甲藻整个细胞周期中脂质合成的动态变化。尼罗红染色细胞的流式细胞图显示,在甲藻细胞周期中,极性脂质含量呈逐步增加,中性脂质含量呈持续增加。抑制脂质合成后,在G1早期观察到细胞周期延迟,但在G2/M期未观察到。然而,在细胞周期停滞于G1/S转换时,脂质合成仍在继续。在细胞周期的G1晚期之后添加纤维素合成抑制剂和脂肪酸合成抑制剂时,未观察到细胞周期延迟。这意味着在甲藻细胞周期的G1晚期存在一个监测脂肪酸合成的关键节点。培养基中葡萄糖浓度的降低下调了G1期细胞大小,同时关键节点向前移动。抑制脂质合成会上调纤维素合成,并导致纤维素含量增加,而抑制纤维素合成对脂质合成没有影响。脂肪酸合成和纤维素合成显然通过独立的途径与细胞周期耦合。

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