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HIM-17-GFP LC-MS/MS analysis in C. elegans

ABSTRACT: HIM-17 has been implicated in the regulation of DNA double-strand break (DSB) formation during meiosis in C. elegans. In a study assessing various accessory factors involved in programmed meiotic DSB formation we show data identifying protein interactions with HIM-17 obtained by assessing HIM-17-GFP pull-downs by LC-MS/MS analysis.

INSTRUMENT(S):

ORGANISM(S): Caenorhabditis Elegans

TISSUE(S): Whole Body

SUBMITTER: Monica Colaiacovo

LAB HEAD: Monica Paola Colaiacovo

PROVIDER: PXD057629 | Pride | 2026-01-28

REPOSITORIES: Pride

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			Action	DRS
	44848.mzXML	Mzxml
	44848.raw	Raw
	44850.mzXML	Mzxml
	44850.raw	Raw
	45617.mzXML	Mzxml

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Publications

Genetic and physical interactions reveal overlapping and distinct contributions to meiotic double-strand break formation in <i>C. elegans</i>.

Raices Marilina M Balmir Fabiola F Silva Nicola N Li Wei W Grundy McKenzie K MK Hoffman Dane K DK Altendorfer Elisabeth E Camacho Carlos Jaime CJ Bernstein Kara A KA Colaiácovo Monica P MP Yanowitz Judith L JL

bioRxiv : the preprint server for biology 20251125

Double-strand breaks (DSBs) are the most deleterious lesions experienced by our genome. Yet, DSBs are intentionally induced during gamete formation to promote the exchange of genetic material between homologous chromosomes. While the conserved topoisomerase-like enzyme Spo11 catalyzes DSBs, additional regulatory proteins-referred to as "Spo11 accessory factors"- regulate the number, timing, and placement of DSBs during meiotic prophase ensuring that SPO11 does not wreak havoc on the genome. Desp ...[more]

PMID: 38463951

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Spo11-oligo mapping in bas1 and ino4 mutants

Project description:Meiotic recombination is initiated by developmentally programmed DNA double-strand breaks (DSBs). In S. cerevisiae, the vast majority of DSBs occur in the nucleosome-depleted regions at gene promoters, where transcription factors (TFs) bind. It has been proposed that TF binding can stimulate DSB formation nearby by modulating local chromatin structure. However, a prior study in TF bas1 mutant suggested that the role of TF binding in determining break formation is complex. Here, we examined fine-scale DSB distributions in TF mutant (bas1Δ and ino4Δ) strains. In bas1Δ mutants, 239 out of the 2468 hotspots showed reduced DSB activity, whereas 87 hotspots showed increased DSB activity. Similarly, in ino4Δ mutant, 415 out of the 2468 hotspots showed reduced DSB activity, whereas 322 hotspots showed increased DSB activity. We also mapped Bas1 and Ino4 binding sites in meiosis and found that only a small portion of the affected hotspots contained TF binding sites. This indicates that TF can influence DSB distribution both directly and indirectly. Surprisingly, these DSB changes in TF mutants did not correlate with change in chromatin structure and histone H3K4me3 modification, suggesting that the role of TF on DSB distribution cannot be simply explained by affecting local chromatin status. Nine samples total: two wild type, four bas1 mutant and three ino4 mutant (each an independent culture)

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