dorsal/arxiv
View SchemaGene Copy Number and Cell Cycle Arrest
| Authors | Bhaswar Ghosh, Indrani Bose |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0510012 |
| URL | https://arxiv.org/abs/q-bio/0510012 |
| DOI | 10.1088/1478-3975/3/1/003 |
Abstract
The cell cycle is an orderly sequence of events which ultimately lead to the division of a single cell into two daughter cells. In the case of DNA damage by radiation or chemicals, the damage checkpoints in the $G_{1}$ and $G_{2}$ phases of the cell cycle are activated. This results in an arrest of the cell cycle so that the DNA damage can be repaired. Once this is done, the cell continues with its usual cycle of activity. We study a mathematical model of the DNA damage checkpoint in the $G_{2}$ phase which arrests the transition from the $G_{2}$ to the $M$ (mitotic) phase of the cell cycle. The tumor suppressor protein p53 plays a key role in activating the pathways leading to cell cycle arrest in mammalian systems. If the DNA damage is severe, the p53 proteins activate other pathways which bring about apoptosis, i.e., programmed cell death. Loss of the p53 gene results in the proliferation of cells containing damaged DNA, i.e., in the growth of tumors which may ultimately become cancerous. There is some recent experimental evidence which suggests that the mutation of a single copy of the p53 gene (in the normal cell each gene has two identical copies) is sufficient to trigger the formation of tumors. We study the effect of reducing the gene copy number of the p53 and two other genes on cell cycle arrest and obtain results consistent with experimental observations.
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"abstract": "The cell cycle is an orderly sequence of events which ultimately lead to the\ndivision of a single cell into two daughter cells. In the case of DNA damage by\nradiation or chemicals, the damage checkpoints in the $G_{1}$ and $G_{2}$\nphases of the cell cycle are activated. This results in an arrest of the cell\ncycle so that the DNA damage can be repaired. Once this is done, the cell\ncontinues with its usual cycle of activity. We study a mathematical model of\nthe DNA damage checkpoint in the $G_{2}$ phase which arrests the transition\nfrom the $G_{2}$ to the $M$ (mitotic) phase of the cell cycle. The tumor\nsuppressor protein p53 plays a key role in activating the pathways leading to\ncell cycle arrest in mammalian systems. If the DNA damage is severe, the p53\nproteins activate other pathways which bring about apoptosis, i.e., programmed\ncell death. Loss of the p53 gene results in the proliferation of cells\ncontaining damaged DNA, i.e., in the growth of tumors which may ultimately\nbecome cancerous. There is some recent experimental evidence which suggests\nthat the mutation of a single copy of the p53 gene (in the normal cell each\ngene has two identical copies) is sufficient to trigger the formation of\ntumors. We study the effect of reducing the gene copy number of the p53 and two\nother genes on cell cycle arrest and obtain results consistent with\nexperimental observations.",
"arxiv_id": "q-bio/0510012",
"authors": [
"Bhaswar Ghosh",
"Indrani Bose"
],
"categories": [
"q-bio.MN",
"q-bio.OT"
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"doi": "10.1088/1478-3975/3/1/003",
"title": "Gene Copy Number and Cell Cycle Arrest",
"url": "https://arxiv.org/abs/q-bio/0510012"
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