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Related Concept Videos

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
The DNA Replication Fork01:02

The DNA Replication Fork

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 forks, one in...
The DNA Replication Fork01:02

The DNA Replication Fork

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 forks, one in...
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.

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Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique
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Published on: October 27, 2011

Rbf1 degron dysfunction enhances cellular DNA replication.

Nitin Raj1, Liang Zhang, Yiliang Wei

  • 1Program in Genetics, Michigan State University, East Lansing, MI, USA.

Cell Cycle (Georgetown, Tex.)
|August 17, 2012
PubMed
Summary
This summary is machine-generated.

The COP9 signalosome stabilizes E2F1 by protecting it from degradation. Mutations disrupting this regulation may promote cancer by enhancing cell cycle progression.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The E2F transcription factor family drives oncogenesis by activating cell proliferation genes.
  • The Retinoblastoma tumor suppressor protein (RB) opposes E2F activity and stabilizes E2F1 by inhibiting its degradation.
  • The physiological consequences of RB-mediated E2F1 stabilization are not fully understood.

Purpose of the Study:

  • To investigate the mechanism and relevance of E2F1 stabilization by RB in Drosophila.
  • To elucidate the role of the COP9 signalosome in regulating E2F1 stability and turnover.

Main Methods:

  • Studied the Rbf1-dE2F1 network in Drosophila during embryonic development.
  • Investigated the interaction between the COP9 signalosome, Cullin4-E3 ligase, and Rbf1.
  • Utilized mutant forms of Rbf1 lacking a C-terminal degron to assess functional properties.

Main Results:

  • The COP9 signalosome protects Rbf1 from degradation and also protects the Cullin4-E3 ligase that degrades dE2F1.
  • This dual role of the COP9 signalosome buffers E2F levels, balancing turnover and stabilization.
  • Rbf1's ability to stabilize dE2F1 is distinct from its gene repression function; removing a degron impaired repression but not stabilization.
  • Mutant Rbf1 lacking the degron enhanced cell cycle progression, mimicking oncogenic transformation.

Conclusions:

  • The COP9 signalosome plays a critical role in regulating E2F1 stability through a dual protective mechanism.
  • Distinct domains of Rbf1 mediate stabilization and gene repression, with the C-terminal degron crucial for repression.
  • Disruption of Rbf1's regulatory domains can lead to enhanced cell proliferation, providing insights into cancer development.