Context-dependent effects of Acf1 assessed in high throughput
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE106759 | GEO | 2017/11/10
SECONDARY ACCESSION(S): PRJNA417865
REPOSITORIES: GEO
Similar Datasets
Project description:The chromatin remodeling complexes CHRAC and ACF combine the ATPase ISWI with the signature subunit ACF1. These enzymes catalyze well-studied nucleosome sliding reactions in vitro, but how their actions affect physiological gene expression is unclear. Here we explored the influence of Drosophila CHRAC/ACF on transcription by complementary gain- and loss-of-function approaches. Targeting ACF1 to multiple reporter genes inserted at many different genomic locations revealed a context-dependent inactivation of poorly transcribed reporters in repressive chromatin. Accordingly, single-embryo transcriptome analysis of a Acf knock-out allele showed that only lowly expressed genes are de-repressed in the absence of ACF1. Finally, the nucleosome arrays in Acf-deficient chromatin show loss of physiological regularity, particularly in transcriptionally inactive domains. Taken together our results highlight that ACF1-containing remodeling factors contribute to the establishment of an inactive ground state of the genome through chromatin organization.
2018-02-05 | GSE106732 | GEO
Project description:The chromatin remodeling complexes CHRAC and ACF combine the ATPase ISWI with the signature subunit ACF1. These enzymes catalyze well-studied nucleosome sliding reactions in vitro, but how their actions affect physiological gene expression is unclear. Here we explored the influence of Drosophila CHRAC/ACF on transcription by complementary gain- and loss-of-function approaches. Targeting ACF1 to multiple reporter genes inserted at many different genomic locations revealed a context-dependent inactivation of poorly transcribed reporters in repressive chromatin. Accordingly, single-embryo transcriptome analysis of a Acf knock-out allele showed that only lowly expressed genes are de-repressed in the absence of ACF1. Finally, the nucleosome arrays in Acf-deficient chromatin show loss of physiological regularity, particularly in transcriptionally inactive domains. Taken together our results highlight that ACF1-containing remodeling factors contribute to the establishment of an inactive ground state of the genome through chromatin organization.
2018-02-05 | GSE106731 | GEO
Project description:Context-dependent effects of Acf1 assessed in high throughput
| PRJNA417865 | ENA
Project description:The nature of chromatin as regular succession of nucleosomes has gained iconic status. The average nucleosome repeat length (NRL) determined by classical means serves as index for bulk chromatin of a given specimen. However, this value is dominated by regular heterochromatin since nucleosomal arrays are often not regular at individual single copy sequences. To obtain a measure for nucleosome regularity in euchromatin we subjected nucleosome dyad profiles to autocorrelation and spectral density analyses. This revealed variation in nucleosome regularity and NRL at different types of euchromatin and yielded a comprehensive catalog of regular phased nucleosome arrays (PNA). The absence of the nucleosome sliding factor ACF1 correlated with global loss of regularity in euchromatin and increased NRL and compromised phasing at a novel type of PNA. Our approach is generally applicable to characterize hallmarks of euchromatin organization.
2018-01-01 | GSE85404 | GEO
Project description:The nature of chromatin as regular succession of nucleosomes has gained iconic status. The average nucleosome repeat length (NRL) determined by classical means serves as index for bulk chromatin of a given specimen. However, this value is dominated by regular heterochromatin since nucleosomal arrays are often not regular at individual single copy sequences. To obtain a measure for nucleosome regularity in euchromatin we subjected nucleosome dyad profiles to autocorrelation and spectral density analyses. This revealed variation in nucleosome regularity and NRL at different types of euchromatin and yielded a comprehensive catalog of regular phased nucleosome arrays (PNA). The absence of the nucleosome sliding factor ACF1 correlated with global loss of regularity in euchromatin and increased NRL and compromised phasing at a novel type of PNA. Our approach is generally applicable to characterize hallmarks of euchromatin organization.
2018-01-01 | GSE85406 | GEO
Project description:The nature of chromatin as regular succession of nucleosomes has gained iconic status. The average nucleosome repeat length (NRL) determined by classical means serves as index for bulk chromatin of a given specimen. However, this value is dominated by regular heterochromatin since nucleosomal arrays are often not regular at individual single copy sequences. To obtain a measure for nucleosome regularity in euchromatin we subjected nucleosome dyad profiles to autocorrelation and spectral density analyses. This revealed variation in nucleosome regularity and NRL at different types of euchromatin and yielded a comprehensive catalog of regular phased nucleosome arrays (PNA). The absence of the nucleosome sliding factor ACF1 correlated with global loss of regularity in euchromatin and increased NRL and compromised phasing at a novel type of PNA. Our approach is generally applicable to characterize hallmarks of euchromatin organization.
2018-01-01 | GSE85405 | GEO
Project description:Acidovorax phage ACF1 Genome sequencing and assembly
| PRJNA745195 | ENA
Project description:ACF1 regulates nucleosome spacing in Drosophila euchromatin
| PRJNA338337 | ENA
Project description:We applied ChIP-seq to map the chromosomal binding sites for two nucleosome remodeling complexes containing the ATPase ISWI, ACF and RSF, in Drosophila embryos. Employing a panel of polyclonal and monoclonal antibodies directed against their signature subunits, ACF1 and RSF1, robust profiles were obtained indicating that both remodelers co-occupied a large set of active promoters. For further validation we repeated the mapping using chromatin of mutant embryos that do not express ACF1 or RSF1. Surprisingly, the ChIP-seq profiles were unchanged, suggesting that they were not due to specific immunoprecipitation. Conservative analysis lists about 3000 chromosomal loci, mostly active promoters that are prone to non-specific enrichment in ChIP and give rise to ‘Phantom Peaks’. These peaks are not obtained with pre-immune serum and are not prominent in input chromatin. Examination of various ACF1 and RSF1 antibodies in Drosophila melanogaster embryos which are wildtype or mutant for the antibody targets.
2015-07-10 | E-GEOD-67323 | biostudies-arrayexpress
Project description:Acf1 was isolated almost 15 years ago from Drosophila embryo extracts as a subunit of several complexes that possess chromatin assembly activity. Acf1 binds to the ATPase ISWI (SNF2H in mammals) to form the ACF/CHRAC chromatin remodeling complexes. Studies in Drosophila and in human and mouse cell culture implicate Acf1 in many cellular processes including transcriptional repression, heterochromatin formation and replication, and DNA damage checkpoints and repair. However, the in vivo function of Acf1 in mammals is unknown. We generated mice deficient for Baz1a, the mammalian homolog of Drosophila Acf1. In contrast to partially penetrant lethality of the mutation in flies, Baz1a-deficient mice are viable. The mutant mice show no obvious defects in B or T cell lineages, class switch recombination in cultured B cells, or meiotic recombination. Thus, BAZ1A is dispensable in vivo for the survival and differentiation of cells that require the repair of developmentally programmed DNA double-strand breaks (DSBs). However, Baz1a-/- male mice are sterile because of a severe defect in spermiogenesis that results in fewer and non-motile sperm with morphological defects. Baz1a-deficient round spermatids display widespread perturbation of gene expression. The mutant cells faithfully execute the widespread reprogramming of gene expression that normally accompanies the developmental transition from meiosis to postmeiotic differentiation, but overlaid on this normal developmental program is mis-regulation of a large number of additional genes. The inappropriate expression of this eclectic group of genes is likely the cause of the pleiotropic spermiogenesis defects in the mutant. We propose that the dramatic changes in chromatin composition that occur in late meiotic prophase and early spermiogenesis create a window of vulnerability during which BAZ1A-targeted chromatin assembly functions are needed to prevent inappropriate transcription changes. This appears to be the sole essential function of the ACF and CHRAC complexes in mouse. total RNA isolated from FACS-enriched pachytene/diplotene spermatocytes and round spermatids from three littermate pairs of Baz1a-/- and Baz1a-/+ animals. Data from all samples are provided, but expression data for one Baz1a-/- spermatocyte sample (683_PD) was censored because of inferred high degree of contamination with round spermatids
2013-11-12 | E-GEOD-41303 | biostudies-arrayexpress