【求助】细胞周期阻滞在G2/M期
丁香园论坛
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请教大家一个问题，我在药物处理后测定细胞的周期，随着药物浓度的增加，G2/M期比例增加（明显，浓度依赖），S期几乎没有变化，而G1期比例减少。是不是说明细胞阻滞在G2/M期？但是G1期和S期的现象怎么解释呢？随后我们测了凋亡，证明药物可以促进细胞凋亡，这些需要怎么联系到一起呢，第一次做，有好多不明白的地方，希望研究周期和凋亡的战友们帮忙分析一下，有没有哪些相关的文献？谢谢大家~
细胞周期被阻滞在G2/M期也是说你的药物是阻滞了细胞周期的进行，不利于细胞的增殖;跟你的凋亡结果是正相关的！
当细胞接收到信号说现在不利于分裂，或者时机不成熟，细胞就会在细胞周期的check point停下来，进行检查。
当时机成熟时，就继续分裂。当检查发现出现无法修复的错误时，细胞就会启动凋亡程序。
The G2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms ranging from yeast to mammals. This checkpoint insures that cells don't initiate mitosis before they have a chance to repair damaged DNA after replication. Cells that have a defective G2-M checkpoint enter mitosis before repairing their DNA, leading to death after cell division.
The cell cycle is driven by proteins called cyclin dependent kinases that associate with cyclin regulatory proteins at different points of the cell cycle. Accumulation of cyclin B increases the activity of the cyclin dependent kinase cdc2 as cells prepare to enter mitosis. Cdc2 activity is further regulated by phosphorylation of its tyrosine-15 residue by the kinase wee1. Phosphorylation of tyrosine-15 inhibits cdc2 activity while dephosphorylation by the phosphatase cdc25 activates the mitotic kinase.
Proteins that localize to sites of DNA damage in G2 initiate a signaling cascade that regulates wee1 and cdc25 activity, therefore controlling mitotic entry via cdc2-cyclin B. Delay in mitotic entry is important for cells to repair any DNA damage that may have accumulated after S phase. Absence of wee1 or removal of the tyrosine-15 site removes negative regulation of cdc2 activity and causes cells to enter mitosis without completing repair, which effectively abolishes the G2-M checkpoint Absence of cdc25 arrests cells in G2, but still allows activation of the G2-M checkpoint, implicating activation of wee1 and deactivation of cdc25 as important regulatory steps in the checkpoint。
附文献2篇参考。
good luck!
当时机成熟时，就继续分裂。当检查发现出现无法修复的错误时，细胞就会启动凋亡程序。
The G2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms ranging from yeast to mammals. This checkpoint insures that cells don't initiate mitosis before they have a chance to repair damaged DNA after replication. Cells that have a defective G2-M checkpoint enter mitosis before repairing their DNA, leading to death after cell division.
The cell cycle is driven by proteins called cyclin dependent kinases that associate with cyclin regulatory proteins at different points of the cell cycle. Accumulation of cyclin B increases the activity of the cyclin dependent kinase cdc2 as cells prepare to enter mitosis. Cdc2 activity is further regulated by phosphorylation of its tyrosine-15 residue by the kinase wee1. Phosphorylation of tyrosine-15 inhibits cdc2 activity while dephosphorylation by the phosphatase cdc25 activates the mitotic kinase.
Proteins that localize to sites of DNA damage in G2 initiate a signaling cascade that regulates wee1 and cdc25 activity, therefore controlling mitotic entry via cdc2-cyclin B. Delay in mitotic entry is important for cells to repair any DNA damage that may have accumulated after S phase. Absence of wee1 or removal of the tyrosine-15 site removes negative regulation of cdc2 activity and causes cells to enter mitosis without completing repair, which effectively abolishes the G2-M checkpoint Absence of cdc25 arrests cells in G2, but still allows activation of the G2-M checkpoint, implicating activation of wee1 and deactivation of cdc25 as important regulatory steps in the checkpoint。
附文献2篇参考。
good luck!
谢谢两位战友的宝贵意见，受益匪浅~
有意思
很简单的一句话：DNA损伤了需要修复。
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