The Caenorhabditis elegansRAD51 homolog is transcribed  into two alternative mRNAs potentially encoding proteins  of different sizes

Rinaldo, Cinzia; Ederle, Sara; Rocco, Vincenzo; Volpe, Adriana La

doi:10.1007/s004380050897

Cited by 23 publications

(18 citation statements)

References 20 publications

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“…The dpy-13 mutation was used as a phenotypic marker to identify rad-51 homozygotes. RAD-51 is the C. elegans homolog of the bacterial RecA protein, which has a crucial role in homologous recombination (Rinaldo et al 1998). In C. elegans, rad-51 has a maternal-effect lethal phenotype.…”

Section: à10mentioning

confidence: 99%

Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 inCaenorhabditis elegans

2006

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In C. elegans, DOG-1 prevents deletions that initiate in polyG/polyC tracts (G/C tracts), most likely by unwinding secondary structures that can form in G/C tracts during lagging-strand DNA synthesis. We have used the dog-1 mutant to assay the in vivo contribution of various repair genes to the maintenance of G/C tracts. Here we show that DOG-1 and the BLM ortholog, HIM-6, act synergistically during replication; simultaneous loss of function of both genes results in replicative stress and an increase in the formation of small deletions that initiate in G/C tracts. Similarly, we demonstrate that the C. elegans orthologs of the homologous recombination repair genes BARD1, RAD51, and XPF and the trans-lesion synthesis polymerases polh and polk contribute to the prevention of deletions in dog-1 mutants. Finally, we provide evidence that the small deletions generated in the dog-1 background are not formed through homologous recombination, nucleotide excision repair, or nonhomologous end-joining mechanisms, but appear to result from a mutagenic repair mechanism acting at G/C tracts. Our data support the hypothesis that absence of DOG-1 leads to replication fork stalling that can be repaired by deletion-free or deletion-prone mechanisms.

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Section: à10mentioning

confidence: 99%

Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 inCaenorhabditis elegans

2006

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“…The C. elegans genome project revealed that C. elegans has two RecA homologs, one of which, Y43C5A.6, is closely related to rad-51 and termed both Ce -rad-51 and Ce-rdh1 (Rinaldo et al 1998;Takanami et al 1998). The other RecA homolog (C30A5.2), the inactivation of which by RNA interference (RNAi) or by transgene cosuppression did not show a distinct phenotype, is related to mammalian rad-51C and was shown to interact with RAD-51 in a two-hybrid assay (Boulton et al 2002;Anton Gartner, unpublished).…”

Section: Introductionmentioning

confidence: 99%

Genetic and cytological characterization of the recombination protein RAD-51 in Caenorhabditis elegans

et al. 2003

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We investigated the role of Caenorhabditis elegans rad-51 during meiotic prophase. We showed that rad-51 mutant worms are viable, have no defects in meiotic homology recognition and synapsis but exhibit abnormal chromosomal morphology and univalent formation at diakinesis. During meiosis RAD-51 becomes localized to distinct foci in nuclei of the transition zone of the gonad and is most abundant in nuclei at late zygotene/early pachytene. Foci then gradually disappear from chromosomes and no foci are observed in late pachytene. RAD-51 localization requires the recombination genes spo-11 and mre-11 as well as chk-2, which is necessary for homology recognition and presynaptic alignment. Mutational analysis with synapsis- and recombination-defective strains, as well as the analysis of strains bearing heterozygous translocation chromosomes, suggests that presynaptic alignment may be required for RAD-51 focus formation, whereas homologous synaptonemal complex formation is required to remove RAD-51 foci.

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“…2 The Caenorhabditis elegans germ line exhibits a complete time course of meiotic prophase in which nuclei at the different stages of oogenesis can be easily identified based on their position and appearance, and it has been shown that DSB repair is differently modulated along the germ line. For example, loading of RAD-51, the only RecA-like protein responsible for the strand exchange step in C. elegans meiosis, 3,4 is RAD-50 independent in the premeiotic region of the germ line and in late-pachytene nuclei, 5 but it is RAD-50 dependent during early meiotic prophase (leptotene to mid-pachytene). During this period, there is a clear bias towards repair using the homologous chromosome as a template, thus promoting CO formation.…”

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Pro-crossover factors regulate damage-dependent apoptosis in the Caenorhabditis elegans germ line

et al. 2013

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During meiosis, DNA double-strand breaks (DSBs) are physiologically induced to start the recombination process and promote the formation of interhomologue crossovers (COs), which are required to ensure faithful chromosome segregation into the gametes. The timely repair of DSBs is an essential part of the meiotic programme, as accumulation of unprocessed DSBs during the pachytene stage of meiotic prophase triggers a DNA damage checkpoint response that induces apoptosis of damaged cells. We show that CO-promoting factors MSH-4, MSH-5, and ZHP-3, but not COSA-1, are required for the apoptotic response of the meiotic DNA damage checkpoint. Lack of MSH-4 or MSH-5 suppresses the apoptotic response observed in some DNA repairdefective mutants such as fcd-2 and brc-1 (orthologues of FANCD2 and BRCA1), irrespectively of the amount of DSBs present in pachytene nuclei. Although ionizing radiation fails to induce apoptosis in msh-4/5-mutant backgrounds, it induces transcriptional activation of the apoptosis-activator egl-1, which is controlled by the Caenorhabditis elegans p53 orthologue CEP-1. This finding suggests that MSH-4/5 involvement in the apoptotic response occurs downstream or independently of damage sensing and checkpoint activation. This study establishes a role for pro-CO factors MSH-4/5 and ZHP-3 in the execution of apoptosis at late meiotic prophase following the accumulation of exogenous or endogenous DNA damage. Cell Death and Differentiation (2013) 20, 1209-1218; doi:10.1038/cdd.2013.68; published online 5 July 2013Eukaryotes execute meiosis to ensure the proper partition of chromosomes into the gametes. Crossing-overs (COs) between homologous chromosomes are essential, along with sister chromatid cohesion, to ensure proper chromosome segregation at meiosis I. All studied organisms exhibit an excess of double-strand breaks (DSBs), generated by type II topoisomerase-like SPO-11, with just a few being ultimately repaired as interhomologue COs. Once DSBs arise, they undergo resection to produce single-stranded DNA, a substrate for the loading of the recombinase RAD-51. This protein, homologous to the Escherichia coli recombinase RecA, promotes strand exchange and invasion of the homologous DNA template, allowing homologous DNA repair to take place. 1 Faithful repair of DSBs during meiosis is crucial to maintain genomic integrity and to allow formation of functional gametes, as unrepaired DSBs trigger activation of the DNA damage checkpoint, which results in a block to cell cycle progression or removal of damaged cells by apoptosis. 2 The Caenorhabditis elegans germ line exhibits a complete time course of meiotic prophase in which nuclei at the different stages of oogenesis can be easily identified based on their position and appearance, and it has been shown that DSB repair is differently modulated along the germ line. For example, loading of RAD-51, the only RecA-like protein responsible for the strand exchange step in C. elegans meiosis, 3,4 is RAD-50 independent in the premeiotic region of the germ line an...

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The Caenorhabditis elegansRAD51 homolog is transcribed into two alternative mRNAs potentially encoding proteins of different sizes

Cited by 23 publications

References 20 publications

Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 inCaenorhabditis elegans

Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 inCaenorhabditis elegans

Genetic and cytological characterization of the recombination protein RAD-51 in Caenorhabditis elegans

Pro-crossover factors regulate damage-dependent apoptosis in the Caenorhabditis elegans germ line

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