Format

Send to

Choose Destination
Genetics. 2018 Aug;209(4):1017-1028. doi: 10.1534/genetics.118.301152. Epub 2018 Jun 8.

A Role in Apoptosis Regulation for the rad-51 Gene of Caenorhabditis elegans.

Author information

1
Institute of Biosciences and BioResources, National Research Council, 80131 Naples, Italy.
2
University of Campania "Luigi Vanvitelli," 81100 Caserta, Italy.
3
Institute of Biosciences and BioResources, National Research Council, 80131 Naples, Italy adele.adamo@ibbr.cnr.it.

Abstract

The evolutionarily conserved RAD-51 protein is essential for homologous recombination in the germ line as well as homologous repair of DNA double-strand breaks in all eukaryotic cells. In the nematode Caenorhabditis elegans, the rad-51 gene is transcribed into messenger RNAs potentially coding three alternative protein isoforms. Null rad-51 alleles display embryonic lethality, severe defects in chromosome structure, and high levels of germ line apoptosis. To dissect its functions, we genetically modified the C. elegans rad-51 gene by clustered regularly interspaced short palindromic repeats/Cas9 genome-editing technology, obtaining a separation-of-function (sfi-) mutant allele that only disrupts the long-transcript isoform. This mutant shows no defects in an otherwise wild-type meiosis and is able to activate physiological germ cell death, which occurs at the late pachytene stage. However, although the mutant is competent in DNA damage checkpoint activation after exposure to ionizing radiation, it is defective for induction of DNA damage-induced apoptosis in meiotic germ cells. These results suggest that RAD-51 plays a novel role in germ line apoptosis independent of RAD-51-mediated strand invasion for homologous recombination.

KEYWORDS:

C. elegans; apoptosis; genome instability; homologous recombination; meiosis

PMID:
29884745
PMCID:
PMC6063241
[Available on 2019-08-01]
DOI:
10.1534/genetics.118.301152
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center