Cells divide and multiply in number as they proceed through the cell cycle. At some point however cells need to stop multiplying and the cell cycle is halted. Given your knowledge on mitosis think of two ways (methods, mechanisms procedures) a cell might stop it self from dividing. Solution Cell cycle is hated when there is damage to DNA or there is not proper DNA replication. At these points cell stops dividing. A) DNA damage: When there is damage in DNA then cell cycle stops dividing to facilitating DNA restore pathways. Methods involves are protein kinases of ATM/ATR own family called Tel1/Mec1 in budding yeast and Tel1/Rad3 in fission yeast. These kinases senses DNA damages and phosphorylate variety of proteins that regulate cell cycle development and DNA restore pathways. B) DNA replication: Accurate replication of the thousands and thousands or billions of DNA base pairs in a eukaryotic genomeis essential. Damaged template, protein and poor supply of dNTPs are most of the many obstacles that must be overcome to duplicate genome. All of those situations can stall replication forks. Stalled forks pose threats to genome integrity due to the fact they could rearrange, damage, or fall apart via disassembly of the replication complex .The pathways that respond to replication stress are signal transduction pathways which might be conserved across evolution. Procedure are ATM/ATR of relatives kinases. These kinases collectively with a trimeric checkpoint clamp (termed nine-1-1 complex) and 5-subunit checkpoint clamp loader (Rad17- RFC2-RFC3-RFC4-RFC5) senses stalled replication forks and transmit a checkpoint .One of principal functions of replication checkpoint is to prevent the onset of mitosis via regulating mitotic control proteins which includes Cdc25. But possibly the maximum essential interest of replication checkpoint is to stabilize and protect replication forks eight. The protein kinase Cds1 (human Chk2 homolog; in human, Chk1 is a purposeful Cds1 homolog) is a important effector of the replication checkpoint within the fission yeast. Cds1 is required to prevent stabilization of replication fork in cells deal with hydroxyurea (HU), a ribonucleotide reductase inhibitor that stalls replication by depleting dNTPs. In the budding yeast Saccharomyces cerevisiae, a failure to set off Rad53 (Chk2 homolog) is related to crumble and regression of replication forks.