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Parp3 promotes long-range end joining in murine cells.

Jacob V Layer1, J Patrick Cleary1, Alexander J Brown2

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Proceedings of the National Academy of Sciences of the United States of America
|September 15, 2018
PubMed
Summary

Poly(ADP)ribose polymerase 3 (PARP3) promotes chromosomal rearrangements in mouse cells, unlike classic nonhomologous end-joining factors. PARP3 deficiency shortens deletion lengths at translocation junctions, indicating a role in DNA double-strand break processing.

Keywords:
Parp3nonhomologous end joiningrearrangements

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Chromosomal rearrangements, such as translocations, are critical early events in tumor development.
  • Previous research highlighted species-specific differences in the genetic factors, particularly nonhomologous end-joining (NHEJ) factors, required for rearrangement formation between human and murine cells.
  • Poly(ADP)ribose polymerase 3 (PARP3) was previously shown to promote endonuclease-induced chromosomal rearrangements in human cells.

Purpose of the Study:

  • To investigate the role of PARP3 in promoting chromosomal rearrangements in murine cells.
  • To compare the mechanisms by which PARP3 and PARP1 influence DNA double-strand break processing and rearrangement formation in mouse cells.

Main Methods:

  • Utilized murine embryonic stem cells (mESCs), primary B cells, and tail fibroblasts.
  • Induced chromosomal rearrangements using endonucleases.
  • Analyzed translocation junctions in Parp3-deficient and Parp1-deficient cells.
  • Employed next-generation sequencing to examine Eml4-Alk fusion junctions.

Main Results:

  • PARP3 was found to promote chromosomal rearrangements in murine cells, including translocations in mESCs, class-switch recombination in B cells, and inversions leading to Eml4-Alk fusions in fibroblasts.
  • Cells deficient in PARP3 exhibited shorter deletion lengths at translocation junctions, suggesting PARP3 facilitates DNA double-strand break processing.
  • PARP1 also promotes rearrangement formation, but its absence resulted in longer deletion lengths, implying a role in suppressing DNA double-strand break processing.
  • PARP3 and PARP1 demonstrate distinct roles and phenotypes in promoting chromosomal rearrangements.

Conclusions:

  • PARP3 plays a conserved role in promoting chromosomal rearrangements in both human and murine cells.
  • PARP3 and PARP1 have opposing effects on DNA double-strand break processing during chromosomal rearrangement formation.
  • These findings elucidate the distinct mechanistic contributions of PARP3 and PARP1 to genomic instability and tumorigenesis.