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Related Concept Videos

DNA-only Transposons02:57

DNA-only Transposons

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DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
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Overview of Transposition and Recombination02:13

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Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
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Transposons01:24

Transposons

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Transposons, or "jumping genes," are small mobile genetic elements (MGEs) that range from 700 to 40,000 base pairs in length. They are found in all organisms and can move within the same chromosome or transfer to different chromosomes. In some cases, transposons can also jump between different host DNA molecules, such as plasmids or viruses, contributing to genetic variability.Barbara McClintock first discovered these mobile genetic elements in the 1940s while studying maize genetics, and she...
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Nucleosome Remodeling02:54

Nucleosome Remodeling

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
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Gene Conversion

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Other than maintaining genome stability via DNA repair, homologous recombination plays an important role in diversifying the genome. In fact, the recombination of sequences forms the molecular basis of genomic evolution. Random and non-random permutations of genomic sequences create a library of new amalgamated sequences. These newly formed genomes can determine the fitness and survival of cells. In bacteria, homologous and non-homologous types of recombination lead to the evolution of new...
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Associated Chromosome Trap for Identifying Long-range DNA Interactions
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Mechanisms for Complex Chromosomal Insertions.

Shen Gu1, Przemyslaw Szafranski1, Zeynep Coban Akdemir1

  • 1Department of Molecular & Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America.

Plos Genetics
|November 24, 2016
PubMed
Summary
This summary is machine-generated.

Complex chromosomal insertions, a type of genomic rearrangement, are formed through replication-based mechanisms. These processes can lead to interchromosomal insertions and copy-number variants, impacting genetic stability.

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Area of Science:

  • Genetics
  • Genomics
  • Molecular Biology

Background:

  • Chromosomal insertions are genomic rearrangements comprising ~2% of nonrecurrent copy-number gains.
  • The molecular mechanisms underlying the formation of chromosomal insertions remain largely unknown.

Purpose of the Study:

  • To investigate the molecular mechanisms of complex chromosomal insertion formation.
  • To identify genetic signatures at breakpoint junctions to infer formation mechanisms.

Main Methods:

  • Clinical array comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH) were used to identify cases.
  • High-density aCGH, long-range PCR, and DNA sequencing were employed for fine-mapping breakpoint junctions.
  • Analysis of familial cases with apparently balanced insertions was performed.

Main Results:

  • Microhomologies and templated insertions at breakpoint junctions suggest replication-based mechanisms with template switches.
  • Analysis of 5 families revealed small copy-number variants (CNVs) flanking insertion sites in 3 cases.
  • These findings indicate replicative repair can generate complex interchromosomal insertions.

Conclusions:

  • Replicative repair mechanisms, potentially involving chromothripsis-like chromoanasynthesis, can explain complex interchromosomal insertions.
  • A significant fraction of apparently balanced insertions may harbor small flanking CNVs due to these mechanisms.