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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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DNA replication has three main steps: initiation, elongation, and termination. Replication in prokaryotes begins when initiator proteins bind to the single origin of replication (ori) on the cell's circular chromosome. Replication then proceeds around the entire circle of the chromosome in each direction from the two replication forks, resulting in two DNA molecules.
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Completing genome replication outside of S phase.

Rahul Bhowmick1, Ian D Hickson2, Ying Liu2

  • 1Center for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Panum Institute, Blegdamsvej 3B, 2200 Copenhagen N, Denmark; Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Molecular Cell
|September 16, 2023
PubMed
Summary

Mitotic DNA synthesis (MiDAS) is a DNA repair process that duplicates under-replicated DNA during mitosis. Targeting MiDAS in cancer cells, which heavily rely on this process, may offer new therapeutic strategies.

Keywords:
BIRMiDASMiDAS-seqbreak-induced replicationfragile siteshomologous recombinationmitotic DNA synthesisreplication stress

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Mitotic DNA synthesis (MiDAS) is an unusual DNA replication process occurring during cell division (mitosis).
  • Initially linked to common fragile sites and replication stress (RS), MiDAS is now recognized as a broader salvage pathway for under-replicated DNA.
  • Emerging evidence suggests MiDAS functions as a DNA repair mechanism involving multiple pathways.

Purpose of the Study:

  • To review the causes of replication stress (RS).
  • To identify genomic regions vulnerable to RS.
  • To discuss strategies for completing DNA replication outside of S phase and the therapeutic potential of targeting MiDAS in cancer.

Main Methods:

  • Literature review of existing research on MiDAS, replication stress, and cancer biology.
  • Synthesis of data on genomic instability and DNA repair mechanisms.
  • Analysis of the role of MiDAS in aneuploid cancer cells.

Main Results:

  • Replication stress (RS) can arise from various sources, leading to under-replicated DNA.
  • Specific genomic regions, such as common fragile sites, are particularly susceptible to RS.
  • MiDAS acts as a crucial salvage pathway to complete DNA duplication during mitosis, functioning as a DNA repair process.

Conclusions:

  • MiDAS is a vital DNA repair mechanism that ensures genome integrity under replication stress.
  • Cancer cells exhibit a high reliance on MiDAS, making it a promising target for novel cancer therapies.
  • Targeting MiDAS could represent a new strategy to improve cancer treatment outcomes by exploiting the dependencies of cancer cells.