Synaptonemal Complex Assembly in C. elegans Is Dispensable for Loading Strand-Exchange Proteins but Critical for Proper Completion of Recombination

Colaiácovo, Mónica P.; MacQueen, Amy J.; Martínez-Pérez, Enrique; McDonald, Kent L.; Adamo, Adele; Volpe, Adriana La; Villeneuve, Anne M.

doi:10.1016/s1534-5807(03)00232-6

Cited by 403 publications

(864 citation statements)

References 41 publications

Supporting

Mentioning

806

Contrasting

Unclassified

Order By: Relevance

“…9.4 , lowest panels). The recombination checkpoint can be triggered, even when only a single meiotic chromosome fails to pair (Colaiacovo et al 2003 ;Alpi et al 2003 ;Mets and Meyer 2009 ) . In those pairing defective mutants apoptosis is thought to be triggered by the excessive SPO-11-generated double-strand breaks, which in the absence of a homologous chromosome fail to be repaired (Fig.…”

Section: Meiotic Recombination Checkpoint and Template Preferencementioning

confidence: 99%

Germ Cell Apoptosis and DNA Damage Responses

Bailly

Gartner

2012

Germ Cell Development in C. Elegans

View full text Add to dashboard Cite

In the past 12 years, since the fi rst description of C. elegans germ cell apoptosis, this area of research rapidly expanded. It became evident that multiple genetic pathways lead to the apoptotic demise of germ cells. We are only beginning to understand how these pathways that all require the CED-9/Bcl-2, Apaf-1/CED-4 and CED-3 caspase core apoptosis components are regulated. Physiological apoptosis, which likely accounts for the elimination of more than 50% of all germ cells, even in unperturbed conditions, is likely to be required to maintain tissue homeostasis. The best-studied pathways lead to DNA damage-induced germ cell apoptosis in response to a variety of genotoxic stimuli. This apoptosis appears to be regulated similar to DNA damage-induced apoptosis in the mouse germ line and converges on p53 family transcription factors. DNA damage response pathways not only lead to apoptosis induction, but also directly affect DNA repair, and a transient cell cycle arrest of mitotic germ cells. Finally, distinct pathways activate germ cell apoptosis in response to defects in meiotic recombination and meiotic chromosome pairing.

show abstract

Section: Meiotic Recombination Checkpoint and Template Preferencementioning

confidence: 99%

Germ Cell Apoptosis and DNA Damage Responses

Bailly

Gartner

2012

Germ Cell Development in C. Elegans

View full text Add to dashboard Cite

show abstract

“…TF proteins, have therefore been identified independently in only a limited number of species, namely mammalian species (SYCP1) (Meuwissen et al, 1992), budding yeast (Zip1) (Sym et al, 1993), Drosophila (C(3)G) (Page and Hawley, 2001) and Caenorhabditis (Syp-1 and Syp-2) (Colaia´covo et al, 2003;MacQueen et al, 2002). Despite their lack of amino acid sequence similarity, SYCP1, Zip1 and C(3)G have a similar structure: they are long coiled coil proteins with globular domains at both ends.…”

Section: Transverse Filament Proteins Are Essential For Crossing Overmentioning

confidence: 99%

“…1a). Caenorhabditis Syp-1 and Syp-2 are two short coiled coil proteins, which possibly take the place of a single longer coiled coil protein in other species (Colaia´covo et al, 2003;MacQueen et al, 2002).…”

Section: Transverse Filament Proteins Are Essential For Crossing Overmentioning

confidence: 99%

“…These mutants still initiate meiotic recombination (by induction of DNA double-strand breaks) (de Vries et al, 2005;Colaia´covo et al, 2003;Jang et al, 2003;Storlazzi et al, 1996), and align homologous chromosomes (de Vries et al, 2005; reviewed by Page and Hawley, 2003). However, in all four analyzed species crossover formation is affected in TF-deficient mutants (reviewed by Page and Figure 1.…”

Section: Transverse Filament Proteins Are Essential For Crossing Overmentioning

confidence: 99%

“…Hawley, 2004 andZickler andKleckner, 1999). In Caenorhabditis and Drosophila meiotic crossing over is completely abolished (Colaia´covo et al, 2003;MacQueen et al, 2002;Page and Hawley, 2001), and in mouse almost completely (de Vries et al, 2005). Yeast zip1 null mutants on the other hand, still display about 30% of the wildtype level of crossing over (Sym et al, 1993).…”

Section: Transverse Filament Proteins Are Essential For Crossing Overmentioning

confidence: 99%

See 2 more Smart Citations

Meiotic Transverse Filament Proteins: Essential for Crossing Over

Heyting

2005

Transgenic Res

View full text Add to dashboard Cite

Meiosis is a specialized set of two nuclear divisions, meiosis I and II, by which a diploid cell produces four haploid daughters. After premeiotic DNA replication, homologous chromosomes pair and recombine, and then disjoin at meiosis I. Subsequently, at meiosis II, the sister chromatids of each chromosome segregate. In nearly all eukaryotes, meiotic chromosome pairing culminates in the formation of a ladderlike supramolecular protein structure, the synaptonemal complex (SC) (Page and Hawley, 2004). The rungs of the ladder are known as transverse filaments (TFs). Genes encoding TF proteins have been identified in a limited number of organisms, and their function has been studied by mutational analysis. Although TF proteins show little amino acid sequence conservation, their structure and function are largely conserved. In all analyzed species, TF proteins are required for meiotic reciprocal recombination (crossing over).

show abstract

Depletion of cdc‐25.3, a Caenorhabditis elegans orthologue of cdc25, increases physiological germline apoptosis

2017

View full text Add to dashboard Cite

In Caenorhabditis elegans hermaphrodites, physiological germline apoptosis is higher in cdc-25.3 mutants than in wild-type. The elevated germline apoptosis in cdc-25.3 mutants seems to be induced by accumulation of double-stranded DNA breaks (DSBs). Both DNA damage and synapsis checkpoint genes are required to increase the germline apoptosis. Notably, the number of germ cells that lose P-granule components, PGL-1 and PGL-3, increase in cdc-25.3 mutants, and the increase in germline apoptosis requires the activity of SIR-2.1, a Sirtuin orthologue. These results suggest that elevation of germline apoptosis in cdc-25.3 mutants is induced by accumulation of DSBs, leading to a loss of PGL-1 and PGL-3 in germ cells, which promotes cytoplasmic translocation of SIR-2.1, and finally activates the core apoptotic machinery.

show abstract

Synaptonemal Complex Assembly in C. elegans Is Dispensable for Loading Strand-Exchange Proteins but Critical for Proper Completion of Recombination

Cited by 403 publications

References 41 publications

Germ Cell Apoptosis and DNA Damage Responses

Germ Cell Apoptosis and DNA Damage Responses

Meiotic Transverse Filament Proteins: Essential for Crossing Over

Depletion of cdc‐25.3, a Caenorhabditis elegans orthologue of cdc25, increases physiological germline apoptosis

Contact Info

Product

Resources

About