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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,...
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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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MYC multimers shield stalled replication forks from RNA polymerase.

Daniel Solvie1, Apoorva Baluapuri1,2,3, Leonie Uhl1

  • 1Department of Biochemistry and Molecular Biology, University of Würzburg, Würzburg, Germany.

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|November 24, 2022
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MYC oncoproteins form structures that help cancer cells survive stress by coordinating DNA repair and replication, limiting DNA damage during S-phase.

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Stress Response

Background:

  • MYC oncoproteins are crucial drivers of human tumor development.
  • MYC proteins regulate transcription, DNA replication, and DNA damage repair in normal cells.

Purpose of the Study:

  • To elucidate the mechanisms behind MYC's diverse cellular functions.
  • To investigate the structural changes and functional consequences of MYC perturbation.

Main Methods:

  • Analysis of MYC protein behavior upon perturbation of transcription elongation, mRNA splicing, and proteasome inhibition.
  • Characterization of MYC interactome changes and multimer formation.
  • Localization studies of MYC multimers in relation to stalled replication forks and DNA repair proteins (FANCD2, ATR, BRCA1).

Main Results:

  • MYC dissociates from promoters and forms multimeric structures under cellular stress.
  • MYC multimerization alters its interactome towards transcription termination and RNA processing factors.
  • MYC multimers accumulate near stalled replication forks, interacting with DNA repair proteins and blocking antisense transcription.

Conclusions:

  • MYC multimerization is a ubiquitylation-dependent process triggered by cellular stress.
  • MYC multimers stabilize DNA repair proteins at stalled replication forks, limiting DNA double-strand breaks.
  • MYC multimerization is a key mechanism enabling tumor cell proliferation under stressful conditions.