细胞周期阻滞于g2⼀mm期，怎么研究机制

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 phosphorylationof 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。