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Related Concept Videos

Genome Copying Errors02:46

Genome Copying Errors

DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
Comparing Copy Number Variations and SNPs02:26

Comparing Copy Number Variations and SNPs

Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
Copy number variations or CNVs are the structural variations that cover more than 1kb of DNA sequence. The single nucleotide polymorphism (SNP), on the other hand, is a single nucleotide change or a point mutation that is found in more than 1%...
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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, a...
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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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...
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Gene Duplication and Divergence

The seminal work of Ohno in 1970 popularized the idea of gene duplication and divergence. DNA sequence comparison studies reveal that a large portion of the genes in bacteria, archaebacteria, and eukaryotes was  generated by gene duplication and divergence, indicating its critical role in evolution.
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Detection of Copy Number Alterations Using Single Cell Sequencing
09:45

Detection of Copy Number Alterations Using Single Cell Sequencing

Published on: February 17, 2017

FBXW7 and DNA copy number instability.

Kristin N Byrd1, Bing Huey, Ritu Roydasgupta

  • 1Cancer Research Institute, University of California San Francisco, Box 0808, San Francisco, CA 94143-0808, USA.

Breast Cancer Research and Treatment
|June 26, 2007
PubMed
Summary

FBXW7 (hCDC4) deficiency is linked to genomic instability. This study found FBXW7 copy loss associated with breast cancer instability, but FBXW7 deficiency unlikely drives extensive copy number aberrations in tumors.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • SKP1-cullin-F-box protein (SCF) ubiquitin ligases regulate cell cycle progression.
  • FBXW7 (hCDC4) encodes an F-box protein crucial for SCF ligase function.
  • FBXW7 deficiency has been implicated in genomic instability.

Purpose of the Study:

  • To investigate the association between FBXW7 deficiency and chromosomal instability in breast cancer.
  • To determine if FBXW7 deficiency contributes to genomic alterations in cancer cells.

Main Methods:

  • Screening breast tumors for FBXW7 mutations and copy number alterations using array comparative genomic hybridization (array CGH).
  • Analyzing FBXW7 transcript levels in tumors with copy number loss.
  • Challenging FBXW7-deficient cells with methotrexate to assess genomic alterations in resistant colonies.

Main Results:

  • No FBXW7 mutations were found in screened breast tumors.
  • FBXW7 copy number loss correlated with enhanced genomic instability in the Complex breast tumor subtype.
  • FBXW7 transcript levels were not reduced in tumors with copy loss, suggesting instability may not stem from FBXW7 haploinsufficiency.
  • Methotrexate-resistant cells derived from FBXW7-deficient cells showed minimal copy number alterations.

Conclusions:

  • FBXW7 deficiency is unlikely to be the primary driver of extensive copy number aberrations observed in breast cancer.
  • While FBXW7 copy loss is associated with genomic instability in certain breast cancer subtypes, the mechanism may involve other neighboring genes.
  • Further research is needed to fully elucidate the role of FBXW7 in cancer genome stability.