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秀丽隐杆线虫细胞周期和细胞命运的时序控制。

The temporal control of cell cycle and cell fate in Caenorhabditis elegans.

作者信息

Ambros V

机构信息

Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA.

出版信息

Novartis Found Symp. 2001;237:203-14; discussion 214-20. doi: 10.1002/0470846666.ch16.

DOI:10.1002/0470846666.ch16
PMID:11444045
Abstract

The nematode Caenorhabditis elegans develops through two major phases: the first phase, embryogenesis, consists of a rapid series of cleavage cell divisions leading to morphogenesis of a first stage larva. The second phase is postembryonic development, which consists of developmentally regulated cell cycles that occur during the four larval stages leading to the adult. Precursor cells set aside during embryogenesis divide through stereotypical cell lineage patterns during the four larval stages to generate larval and adult structures. The precise timing of the postembryonic cell divisions is under strict control, in most cases with a developmentally regulated G1. In certain postembryonic cell lineages, various aspects of the cell division cycle, including cell cycle exit, or G1/S progression, are controlled by temporal regulatory genes of the heterochronic gene pathway. Heterochronic genes also control the timing of numerous other developmental events, indicating that this pathway functions to coordinate the schedule of cell division and cellular differentiation throughout the animal. Some choices of cell fate that occur in response to inductive or lateral signals are linked to cell cycle progression, suggesting that cell cycle phase can confer a critical period for developmental potential in certain cells.

摘要

线虫秀丽隐杆线虫的发育经历两个主要阶段

第一阶段是胚胎发生,由一系列快速的卵裂细胞分裂组成,导致第一阶段幼虫的形态发生。第二阶段是胚胎后发育,它由在四个幼虫阶段发生的受发育调控的细胞周期组成,最终发育为成虫。胚胎发生过程中预留的前体细胞在四个幼虫阶段通过定型的细胞谱系模式进行分裂,以生成幼虫和成虫结构。胚胎后细胞分裂的精确时间受到严格控制,在大多数情况下,具有受发育调控的G1期。在某些胚胎后细胞谱系中,细胞分裂周期的各个方面,包括细胞周期退出或G1/S进展,都由异时性基因途径的时间调控基因控制。异时性基因还控制许多其他发育事件的时间,这表明该途径的功能是协调整个动物的细胞分裂和细胞分化时间表。一些因诱导或侧向信号而发生的细胞命运选择与细胞周期进程相关,这表明细胞周期阶段可以赋予某些细胞发育潜能的关键时期。

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1
The temporal control of cell cycle and cell fate in Caenorhabditis elegans.秀丽隐杆线虫细胞周期和细胞命运的时序控制。
Novartis Found Symp. 2001;237:203-14; discussion 214-20. doi: 10.1002/0470846666.ch16.
2
Essential embryonic roles of the CKI-1 cyclin-dependent kinase inhibitor in cell-cycle exit and morphogenesis in C elegans.CKI-1细胞周期蛋白依赖性激酶抑制剂在秀丽隐杆线虫细胞周期退出和形态发生中的重要胚胎作用。
Dev Biol. 2003 Aug 1;260(1):273-86. doi: 10.1016/s0012-1606(03)00239-2.
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Developmental regulation of a cyclin-dependent kinase inhibitor controls postembryonic cell cycle progression in Caenorhabditis elegans.细胞周期蛋白依赖性激酶抑制剂的发育调控控制秀丽隐杆线虫胚胎后期的细胞周期进程。
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Results Probl Cell Differ. 2011;53:109-33. doi: 10.1007/978-3-642-19065-0_6.
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The temporally regulated transcription factor sel-7 controls developmental timing in C. elegans.具有时间调控功能的转录因子sel-7控制线虫的发育时间。
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Timing of Tissue-specific Cell Division Requires a Differential Onset of Zygotic Transcription during Metazoan Embryogenesis.组织特异性细胞分裂的时间安排需要后生动物胚胎发生过程中合子转录的差异起始。
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Nutritional control of postembryonic development progression and arrest in Caenorhabditis elegans.营养控制秀丽隐杆线虫胚胎后发育进程和停滞。
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Organ-specific cell division abnormalities caused by mutation in a general cell cycle regulator in C. elegans.秀丽隐杆线虫中一种通用细胞周期调节因子的突变导致的器官特异性细胞分裂异常。
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Control of developmental timing in Caenorhabditis elegans.秀丽隐杆线虫发育时间的调控
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The CDC-14 phosphatase controls developmental cell-cycle arrest in C. elegans.CDC-14磷酸酶调控秀丽隐杆线虫发育过程中的细胞周期停滞。
Nat Cell Biol. 2004 Aug;6(8):777-83. doi: 10.1038/ncb1154. Epub 2004 Jul 11.

引用本文的文献

1
Systems-level quantification of division timing reveals a common genetic architecture controlling asynchrony and fate asymmetry.细胞分裂时间的系统级定量分析揭示了控制异步性和命运不对称性的共同遗传结构。
Mol Syst Biol. 2015 Jun 10;11(6):814. doi: 10.15252/msb.20145857.
2
The ortholog of the human proto-oncogene ROS1 is required for epithelial development in C. elegans.人类原癌基因ROS1的直系同源基因是秀丽隐杆线虫上皮发育所必需的。
Genesis. 2013 Aug;51(8):545-61. doi: 10.1002/dvg.22405. Epub 2013 Jun 27.
3
Cyclin D regulation of a sexually dimorphic asymmetric cell division.
细胞周期蛋白D对性别二态性不对称细胞分裂的调控。
Dev Cell. 2005 Oct;9(4):489-99. doi: 10.1016/j.devcel.2005.09.004.