Similar Datasets
Project description:Correct chromosome segregation requires that sister chromatids are held together by the protein complex cohesin, from S phase until anaphase. This S phase established cohesion is, together with DSB recruitment of cohesin and formation of damage induced (DI) cohesion, also important for repair of DSBs. Eco1 is a common essential factor for S phase and DI-cohesion. The fission yeast Eco1ortholog, Eso1, is important both for S phase cohesion and for bypass of UV induced lesions, and is expressed as a fusion protein with Polη. The cohesion function has been attributed solely to Eso1 and the lesion bypass function to the Polη part of the protein. As we found the interaction between the two proteins intriguing we decided to look for a functional connection also in budding yeast. Indeed, despite being dispensable for S phase cohesion, budding yeast Polη is required for formation of DI genome-wide cohesion. However, Polη deficient cells are DSB repair competent, revealing differential regulation of DI-cohesion at the break and genome-wide. This finding challenges the importance of DI genome-wide cohesion for DSB repair, and based on our findings we suggest that S phase cohesion is not sufficient for correct chromosome segregation in the presence of DNA damage.
2013-01-15 | GSE42655 | GEO
Project description:Asf1, through its histone chaperone activity, helps chromatin closing/opening during DNA replication, repair, recombination and transcription. Despite extensive research on Asf1-mediated physiological functions, a genome-wide localization map is lacking, limiting our knowledge of chromosomal features targeted by Asf1. We present a high-resolution genome-wide map of Asf1, localizing at essentially all pol III-transcribed genes, highly active pol II-transcribed genes and heterochromatic features. Pol III-transcribed genes are negatively regulated by Asf1, whereas pol II genes are regulated indirectly by Asf1-dependent H3K56 acetylation. Interestingly, Asf1 localization along yeast chromosomes shows nearly identical distribution to that of the condensin complex, predicting a functional overlap in chromosome architecture and genome organization. ChIP-seq analysis of Asf1 targets using a yeast strain that expresses an 18-Myc tag fused to the C-terminus of ASF1. Two biological replicates and one mock/control were performed. The Illumina GAII was used. ChIP-seq reads are aligned to the budding yeast sacCer3 (2011) assembly.
2014-07-30 | E-GEOD-40717 | biostudies-arrayexpress
Project description:Correct chromosome segregation requires that sister chromatids are held together by the protein complex cohesin, from S phase until anaphase. This S phase established cohesion is, together with DSB recruitment of cohesin and formation of damage induced (DI) cohesion, also important for repair of DSBs. Eco1 is a common essential factor for S phase and DI-cohesion. The fission yeast Eco1ortholog, Eso1, is important both for S phase cohesion and for bypass of UV induced lesions, and is expressed as a fusion protein with Polη. The cohesion function has been attributed solely to Eso1 and the lesion bypass function to the Polη part of the protein. As we found the interaction between the two proteins intriguing we decided to look for a functional connection also in budding yeast. Indeed, despite being dispensable for S phase cohesion, budding yeast Polη is required for formation of DI genome-wide cohesion. However, Polη deficient cells are DSB repair competent, revealing differential regulation of DI-cohesion at the break and genome-wide. This finding challenges the importance of DI genome-wide cohesion for DSB repair, and based on our findings we suggest that S phase cohesion is not sufficient for correct chromosome segregation in the presence of DNA damage. Whole Genome binding of G2 expressed Scc1 in the presence and absence of Rad30.
2013-01-15 | E-GEOD-42655 | biostudies-arrayexpress
Project description:Meiotic chromosome architecture called M-bM-^@M-^\axis-loop structuresM-bM-^@M-^] and histone modifications have been demonstrated to regulate the Spo11-dependent formation of DNA double-strand breaks (DSBs) that trigger meiotic recombination. Using genome-wide chromatin immunoprecipitation (ChIP) analyses followed by deep sequencing, we compared the genome-wide distribution of the axis protein Rec8 (the kleisin subunit of meiotic cohesin) with that of oligomeric DNA covalently bound to Spo11, indicative of DSB sites. The frequency of DSB sites is overall constant between Rec8 binding sites. However, DSB cold spots are observed in regions spanning M-BM-10.8 kb around Rec8 binding sites. The axis-associated cold spots are not due to exclusion of Spo11 localization from the axis, since ChIP experiments revealed that substantial Spo11 persists at Rec8 binding sites during DSB formation. Spo11 fused with Gal4 DNA binding domain (Gal4BD-Spo11) tethered in close proximity (M-bM-^IM-$0.8 kb) to Rec8 binding sites hardly forms meiotic DSBs, in contrast with other regions. In addition, H3K4 tri-methylation (H3K4me3) remarkably decreases at Rec8 binding sites. These results suggest that reduced histone H3K4me3 in combination with inactivation of Spo11 activity on the axis discourages DSB hot spot formation. ChIP-seq analyses of Rec8, Spo11, and Gal4BD-Spo11 on budding yeast meiotic chromosomes M-bM-^@M-" Distribution of Rec8 in wt and Gal4BD-Spo11-expressing cells at 4h after meiotic induction M-bM-^@M-" Distribution of Spo11 at 3h, 4h, and 5h after meiotic induction M-bM-^@M-" Distribution of Gal4BD-Spo11 at 0h after meiotic induction
2014-03-31 | E-GEOD-52862 | biostudies-arrayexpress
Project description:Chip-Seq profiles of Hop1 and Red1 in budding yeast
| PRJEB8212 | ENA
Project description:We report the application of ChIP-sequencing technology for high-throughput profiling of histone modifications in budding yeast. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide maps of Set1 and H3K4me3 in yeast cells. We find that Set1 and H3 lysine 4 trimethylation locate primarily in open reading frame of genes. In addition, we focus on the distribution of Set1 and H3K4me3 in histone gene clusters and found strong similar binding of Set1 and H3K4me3 on all histone genes.
2019-05-02 | GSE115910 | GEO
Project description:Determining the genomic localization of chromatin features is an essential aspect of investigating gene expression control, and ChIP-Seq has long been the gold standard technique for interrogating chromatin landscapes. Recently, the development of alternative methods, such as CUT&Tag, have provided researchers with alternative strategies that eliminate the need for chromatin purification, and allow for in situ investigation of histone modifications and chromatin bound factors. Mindful of technical differences, we set out to investigate whether distinct chromatin modifications were equally compatible with these different chromatin interrogation techniques. We found that ChIP-Seq and CUT&Tag performed similarly for modifications known to reside at gene regulatory regions, such as promoters and enhancers, but major differences were observed when we assessed enrichment over heterochromatin-associated loci. Unlike ChIP-Seq, CUT&Tag detects robust levels of H3K9me3 at a substantial number of repetitive elements, with especially high sensitivity over evolutionarily young retrotransposons. IAPEz-int elements for example, exhibited underrepresentation in mouse ChIP-Seq datasets but strong enrichment using CUT&Tag. Additionally, we identified several euchromatin-associated proteins that co-purify with repetitive loci and are similarly depleted when applying ChIP-based methods. This study reveals that our current knowledge of chromatin states across the heterochromatin portions of the mammalian genome is extensively incomplete, largely due to36 limitations of ChIP-Seq. We also demonstrate that newer in situ chromatin fragmentation-based techniques, such as CUT&Tag and CUT&RUN, are more suitable for studying chromatin modifications over repetitive elements and retrotransposons.
2025-08-26 | PXD067760 | Pride
Project description:ChIP-Seq analysis of V5-tagged budding yeast Rif1
| PRJEB67558 | ENA
Project description:ChIP-Seq analysis of Myc-tagged budding yeast Rif1
| PRJEB67557 | ENA