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Related Concept Videos

Single Nucleotide Polymorphisms-SNPs01:05

Single Nucleotide Polymorphisms-SNPs

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A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
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Comparing Copy Number Variations and SNPs02:26

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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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Genetic Variation01:25

Genetic Variation

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Genetic variation is the diversity in DNA sequences found among individuals of the same species. This diversity is crucial for a species' survival because it helps organisms adapt to environmental changes. Genetic variation begins with fertilization, where an egg and sperm cell merge. Each of these cells carries 23 chromosomes, up to 46 in the fertilized egg. Chromosomes are long DNA strands that contain genes, the basic units of heredity.
Genes exist in different versions called alleles,...
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Viral Mutations00:36

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A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
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Leaky Scanning02:28

Leaky Scanning

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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Mutation, Gene Flow, and Genetic Drift01:09

Mutation, Gene Flow, and Genetic Drift

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In a population that is not at Hardy-Weinberg equilibrium, the frequency of alleles changes over time. Therefore, any deviations from the five conditions of Hardy-Weinberg equilibrium can alter the genetic variation of a given population. Conditions that change the genetic variability of a population include mutations, natural selection, non-random mating, gene flow, and genetic drift (small population size).
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Structural Consequences of Variation in SARS-CoV-2 B.1.1.7.

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  • 1Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, USA.

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The UK variant B.1.1.7 of SARS-CoV-2 has mutations enhancing ACE2 binding and replication. These changes in the spike protein may explain increased transmissibility and offer new drug targets.

Keywords:
Angiotensin Converting Enzyme-2Drug discoveryMutationSARS-CoV-2

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Area of Science:

  • Virology
  • Structural Biology
  • Molecular Biology

Background:

  • New SARS-CoV-2 strains raise concerns about transmissibility, fitness, and immune evasion.
  • The UK variant B.1.1.7 (SARS-CoV-2 VUI 202012/01) shows increased transmissibility, potentially due to mutations in its spike protein.

Purpose of the Study:

  • To investigate the functional effects of mutations in the UK variant B.1.1.7 spike protein.
  • To analyze structural changes in the spike protein and their impact on ACE2 binding and viral mechanisms.

Main Methods:

  • 3D modeling of the UK variant B.1.1.7 spike protein.
  • Structural analysis of mutations on the spike glycoprotein trimer complexed to ACE2.

Main Results:

  • Four of nine mutations in B.1.1.7 alter direct intermolecular interactions.
  • N501Y mutation increases spike protein affinity for ACE2.
  • A570D, D614G, and S982A mutations enhance spike protein cleavage and fusion dynamics.

Conclusions:

  • Mutations in B.1.1.7 contribute to high-affinity ACE2 binding and enhanced replication.
  • The D614G mutation may present a druggable target at the S1/S2 subunit interface.