Format

Send to

Choose Destination
Semin Cell Dev Biol. 2016 Jun;54:177-87. doi: 10.1016/j.semcdb.2016.02.019. Epub 2016 Feb 12.

Mechanisms of germ line genome instability.

Author information

1
Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA;. Electronic address: kims5@mskcc.org.
2
Developmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: petersos@mskcc.org.
3
Developmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: m-jasin@ski.mskcc.org.
4
Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA;; Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: s-keeney@ski.mskcc.org.

Abstract

During meiosis, numerous DNA double-strand breaks (DSBs) are formed as part of the normal developmental program. This seemingly destructive behavior is necessary for successful meiosis, since repair of the DSBs through homologous recombination (HR) helps to produce physical links between the homologous chromosomes essential for correct chromosome segregation later in meiosis. However, DSB formation at such a massive scale also introduces opportunities to generate gross chromosomal rearrangements. In this review, we explore ways in which meiotic DSBs can result in such genomic alterations.

KEYWORDS:

Meiosis; Microhomology-mediated end joining (MMEJ); Non-allelic homologous recombination (NAHR); Nonhomologous end joining (NHEJ); Single-strand annealing (SSA); Translocation

PMID:
26880205
DOI:
10.1016/j.semcdb.2016.02.019
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center