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Better living with hyper-mutation.

Myron F Goodman1,2

  • 1Department of Biological Sciences, University of Southern California, Los Angeles, California.

Environmental and Molecular Mutagenesis
|June 9, 2016
PubMed
Summary
This summary is machine-generated.

Hypermutations, or rapid DNA changes, can be beneficial for evolution or harmful, depending on regulation. This study examines hypermutation in E. coli using DNA polymerase V and in humans with activation-induced deoxycytidine deaminase (AID).

Keywords:
AIDDNA polymeraseRecA nucleoprotein filamentSOS mutagenesishypermutationimmunological diversitytranslesion DNA synthesis

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Area of Science:

  • Molecular Biology
  • Genetics
  • Evolutionary Biology

Background:

  • Mutations, especially base substitutions, usually have negative effects but are crucial for evolution.
  • Hypermutations, occurring at high frequencies, present a balance between genetic fitness and cellular death, influenced by regulatory mechanisms.
  • Two key systems exhibiting hypermutation are DNA polymerase V (pol V) in Escherichia coli and activation-induced deoxycytidine deaminase (AID) in humans.

Purpose of the Study:

  • To explore the dual role of hypermutation in genetic diversity and potential harm.
  • To detail the regulatory mechanisms controlling DNA polymerase V activity in E. coli.
  • To investigate the function of activation-induced deoxycytidine deaminase (AID) in human immune system adaptation and its potential risks.

Main Methods:

  • Examined the induction and regulation of DNA polymerase V (pol V) within the SOS regulon in E. coli.
  • Analyzed the role of pol V in translesion DNA synthesis (TLS) and mutation generation in response to DNA damage.
  • Investigated the mechanism of somatic hypermutation (SHM) initiated by AID in human immunoglobulin variable (IgV) regions.

Main Results:

  • Pol V, induced by DNA damage, is a major source of mutations during TLS and is tightly regulated by temporal, internal, conformational, and spatial mechanisms.
  • SOS-induced polymerases can also mutate undamaged DNA, contributing to genetic diversity and long-term evolutionary fitness.
  • AID initiates SHM by deaminating cytosine to uracil in specific DNA motifs, crucial for antibody diversity but can lead to lymphomas if dysregulated.

Conclusions:

  • Hypermutation, exemplified by pol V in E. coli and AID in humans, plays a critical role in both evolutionary adaptation and disease.
  • Tight regulation of hypermutating enzymes is essential to harness their benefits for diversity while preventing detrimental effects like cancer.
  • Understanding these mechanisms is key to comprehending genetic variation, immune system function, and the origins of certain cancers.