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Related Concept Videos

Chromatin Structure Regulates pre-mRNA Processing02:41

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In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
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Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
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A gene is a stretch of DNA that serves as the blueprint for functional RNAs and proteins. Since DNA is comprised  of nucleotides and proteins are comprised of amino acids, a mediator is required to convert the information encoded in DNA into proteins. This mediator is the messenger RNA (mRNA). mRNA copies the blueprint from DNA by a process called transcription. In eukaryotes, transcription occurs in the nucleus by complementary base-pairing with the DNA template. The mRNA is then...
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Sudemycin E influences alternative splicing and changes chromatin modifications.

Paolo Convertini1, Manli Shen, Philip M Potter

  • 1Department of Molecular and Cellular Biochemistry, University of Kentucky, 741 South Limestone, Lexington, KY 40536, USA, Department of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA and GenoSplice Technology, Hôpital Saint-Louis, Av Claude Vellefaux, 75010 Paris, France.

Nucleic Acids Research
|March 14, 2014
PubMed
Summary
This summary is machine-generated.

Sudemycin E, a cancer cell death inducer, targets SF3B1 in U2 small nuclear ribonucleoproteins (snRNPs). It disrupts snRNP-nucleosome interaction, altering splicing and chromatin, leading to cancer cell death.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Sudemycin E is a novel analog of pre-messenger RNA splicing modulators.
  • Its mechanism of cancer cell death induction remains largely unknown.
  • It shares similarities with spliceostatin A, a known modulator of RNA splicing.

Purpose of the Study:

  • To elucidate the molecular mechanism by which Sudemycin E induces cancer cell death.
  • To investigate Sudemycin E's interaction with cellular components involved in RNA splicing and chromatin regulation.
  • To determine the downstream effects of Sudemycin E on gene expression and cell cycle progression.

Main Methods:

  • Chromatin immunoprecipitation assays to study U2 small nuclear ribonucleoprotein (snRNP) interactions with nucleosomes.
  • Genome-wide array analysis to assess changes in gene expression.
  • Analysis of chromatin modifications, specifically H3K36me3, in response to Sudemycin E treatment.

Main Results:

  • Sudemycin E binds to SF3B1, a component of U2 snRNPs.
  • It induces dissociation of U2 snRNPs from nucleosomes, impacting RNA splicing.
  • Treatment leads to altered alternative splicing, changes in gene expression, G2 cell cycle arrest, and loss of H3K36me3 modification.

Conclusions:

  • Sudemycin E interferes with U2 snRNP's role in maintaining H3K36me3 modification on actively transcribed genes.
  • The drug-induced chromatin condensation, resulting from altered splicing and epigenetic modifications, is a likely driver of cancer cell death.
  • Sudemycin E represents a potential therapeutic agent targeting RNA splicing and chromatin dynamics in cancer.