Actin-related protein Arp4 regulates euchromatic gene expression and development by H2A.Z deposition in blood-stage Plasmodium falciparum [H3K9ac ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA602002 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10912252_1.fastq.gz | Fastqsanger.gz | |||
| SRR10912252_2.fastq.gz | Fastqsanger.gz | |||
| SRR10912253_1.fastq.gz | Fastqsanger.gz | |||
| SRR10912253_2.fastq.gz | Fastqsanger.gz | |||
| SRR10912254_1.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin structure is a basal epigenetic mechanism that determines cellular fate by organizing the dynamic gene expression during the cell development and proliferation. The nuclear members of the evolutionarily conserved actin-related protein (ARPs) superfamily are major components of nucleosome remodelingcomplexes in the nucleus. In the human malaria parasites, Plasmodium falciparum, comparative genome analysis reveals that two canonical actins and three orthologues of ARPs including PfArp1, PfArp4, and PfArp6 are encoded in the genome of this parasite. However, little is known about the biological functions of the two nuclear PfArp4 and PfArp6 proteins. Here, by Pfarp4 gene knockdown and comparative transcriptome analysis, we uncovered that PfArp4 correlated positively with the dynamic expression of eukaryotic genes. Genome-wide distribution analysis by ChIP-seq revealed that PfArp4 protein colocalized with the histone 2A variant H2A.Z and euchromatic marker H3K9ac in the intergenic regions. Inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac level at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundances. Moreover, we found a significant enrichment of PfArp4 at the flanking sites of centromeres, which likely shapes the H2A.Z-enriched centromeric chromatin microenvironment as a boundary marker. PfArp4 depletion triggered loss of H2A.Z at the entire centromere regions, and arrested the blood-stage development probably through interference with the schizogony process. Finally, PfArp6 was detected as an interactor of PfArp4 in the nucleus. Taken together, our finding indicates that the nuclear PfArp4/6regulates the cell cycles through controlling H2A.Z deposition and centromere biology, which will contribute to understanding the complex epigenetic regulation of gene expression and development of the malaria parasites.
2020-06-24 | GSE143900 | GEO
Project description:Chromatin structure is a basal epigenetic mechanism that determines cellular fate by organizing the dynamic gene expression during the cell development and proliferation. The nuclear members of the evolutionarily conserved actin-related protein (ARPs) superfamily are major components of nucleosome remodeling complexes in the nucleus. In the human malaria parasites, Plasmodium falciparum, comparative genome analysis reveals that two canonical actins and three orthologues of ARPs including PfArp1, PfArp4, and PfArp6 are encoded in the genome of this parasite. However, little is known about the biological functions of the two nuclear PfArp4 and PfArp6 proteins. Here, by Pfarp4 gene knockdown and comparative transcriptome analysis, we uncovered that PfArp4 correlated positively with the dynamic expression of eukaryotic genes. Genome-wide distribution analysis by ChIP-seq revealed that PfArp4 protein colocalized with the histone 2A variant H2A.Z and euchromatic marker H3K9ac in the intergenic regions. Inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac level at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundances. Moreover, we found a significant enrichment of PfArp4 at the flanking sites of centromeres, which likely shapes the H2A.Z-enriched centromeric chromatin microenvironment as a boundary marker. PfArp4 depletion triggered loss of H2A.Z at the entire centromere regions, and arrested the blood-stage development probably through interference with the schizogony process. Finally, PfArp6 was detected as an interactor of PfArp4 in the nucleus. Taken together, our finding indicates that the nuclear PfArp4/6regulates the cell cycles through controlling H2A.Z deposition and centromere biology, which will contribute to understanding the complex epigenetic regulation of gene expression and development of the malaria parasites.
2020-06-24 | GSE143898 | GEO
Project description:Actin-related protein Arp4 regulates euchromatic gene expression and development by H2A.Z deposition in blood-stage Plasmodium falciparum [Arp4/6 ChIP-seq]
| PRJNA602004 | ENA
Project description:Chromatin structure is a basal epigenetic mechanism that determines cellular fate by organizing the dynamic gene expression during the cell development and proliferation. The nuclear members of the evolutionarily conserved actin-related protein (ARPs) superfamily are major components of nucleosome remodelingcomplexes in the nucleus. In the human malaria parasites, Plasmodium falciparum, comparative genome analysis reveals that two canonical actins and three orthologues of ARPs including PfArp1, PfArp4, and PfArp6 are encoded in the genome of this parasite. However, little is known about the biological functions of the two nuclear PfArp4 and PfArp6 proteins. Here, by Pfarp4 gene knockdown and comparative transcriptome analysis, we uncovered that PfArp4 correlated positively with the dynamic expression of eukaryotic genes. Genome-wide distribution analysis by ChIP-seq revealed that PfArp4 protein colocalized with the histone 2A variant H2A.Z and euchromatic marker H3K9ac in the intergenic regions. Inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac level at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundances. Moreover, we found a significant enrichment of PfArp4 at the flanking sites of centromeres, which likely shapes the H2A.Z-enriched centromeric chromatin microenvironment as a boundary marker. PfArp4 depletion triggered loss of H2A.Z at the entire centromere regions, and arrested the blood-stage development probably through interference with the schizogony process. Finally, PfArp6 was detected as an interactor of PfArp4 in the nucleus. Taken together, our finding indicates that the nuclear PfArp4/6regulates the cell cycles through controlling H2A.Z deposition and centromere biology, which will contribute to understanding the complex epigenetic regulation of gene expression and development of the malaria parasites.
2020-06-24 | GSE143899 | GEO
Project description:Actin-related protein Arp4 regulates euchromatic gene expression and development by H2A.Z deposition in blood-stage Plasmodium falciparum
| PRJNA602001 | ENA
Project description:Chromatin structure is a basal epigenetic mechanism that determines cellular fate by organizing the dynamic gene expression during the cell development and proliferation. The nuclear members of the evolutionarily conserved actin-related protein (ARPs) superfamily are major components of nucleosome remodelingcomplexes in the nucleus. In the human malaria parasites, Plasmodium falciparum, comparative genome analysis reveals that two canonical actins and three orthologues of ARPs including PfArp1, PfArp4, and PfArp6 are encoded in the genome of this parasite. However, little is known about the biological functions of the two nuclear PfArp4 and PfArp6 proteins. Here, by Pfarp4 gene knockdown and comparative transcriptome analysis, we uncovered that PfArp4 correlated positively with the dynamic expression of eukaryotic genes. Genome-wide distribution analysis by ChIP-seq revealed that PfArp4 protein colocalized with the histone 2A variant H2A.Z and euchromatic marker H3K9ac in the intergenic regions. Inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac level at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundances. Moreover, we found a significant enrichment of PfArp4 at the flanking sites of centromeres, which likely shapes the H2A.Z-enriched centromeric chromatin microenvironment as a boundary marker. PfArp4 depletion triggered loss of H2A.Z at the entire centromere regions, and arrested the blood-stage development probably through interference with the schizogony process. Finally, PfArp6 was detected as an interactor of PfArp4 in the nucleus. Taken together, our finding indicates that the nuclear PfArp4/6regulates the cell cycles through controlling H2A.Z deposition and centromere biology, which will contribute to understanding the complex epigenetic regulation of gene expression and development of the malaria parasites.
2020-06-24 | GSE143901 | GEO
Project description:Actin-related protein Arp4 regulates euchromatic gene expression and development by H2A.Z deposition in blood-stage Plasmodium falciparum [H2A.Z ChIP-seq]
| PRJNA602005 | ENA
Project description:Actin-related protein Arp4 regulates euchromatic gene expression and development by H2A.Z deposition in blood-stage Plasmodium falciparum [RNA-seq]
| PRJNA602003 | ENA
Project description:BackgroundMalaria caused by Plasmodium spp. is still a major threat to public health globally. The various approaches to developing new antimalarial agents rely on the understanding of the complex regulatory mechanisms of dynamic gene expression in the life-cycle of these malaria parasites. The nuclear members of the evolutionarily conserved actin-related protein nuclear (ARP) superfamily are the major components of nucleosome remodelling complexes. In the human malaria parasite Plasmodium falciparum, bioinformatics analysis has predicted three ARP orthologues: PfArp1, PfArp4 and PfArp6. However, little is known about the biological functions of putative PfArp4. In this study, we aimed to investigate the function and the underlying mechanisms of PfArp4 gene regulation.MethodsA conditional gene knockdown approach was adopted by incorporating the glucosamine-inducible glmS ribozyme sequence into the 3' UTR of the PfArp4 and PfArp6 genes. The transgenic parasites PfArp4-Ty1-Ribo, PfArp6-Ty1-Ribo and pL6-PfArp4-Ty1::PfArp6-HA were generated by the CRISPR-Cas9 technique. The knockdown effect in the transgenic parasite was measured by growth curve assay and western blot (WB) analysis. The direct interaction between PfArp4 and PfArp6 was validated by co-IFA and co-IP assays. The euchromatic gene expression mediated through H2A.Z (histone H2A variant) deposition and H3K9ac modification at promoters and regulated by PfArp4, was determined by RNA-seq and ChIP-seq.ResultsThe inducible knockdown of PfArp4 inhibited blood-stage development of P. falciparum. PfArp4 and PfArp6 were colocalized in the nucleus of P. falciparum parasites. PfArp4 gene knockdown altered the global transcriptome. PfArp4 protein colocalized with the histone variant H2A.Z and euchromatic marker H3K9ac in intergenic regions. The inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac levels at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundance of H2A.Z-dependent genes.ConclusionsOur findings suggest that PfArp4 regulates the cell cycle by controlling H2A.Z deposition and affecting centromere function, contributing to the understanding the complex epigenetic regulation of gene expression and the development of P. falciparum.
| S-EPMC7301494 | biostudies-literature
Project description:The actin-related proteins (ARPs) comprise a conserved protein family. Arp4p is found in large multisubunits of the INO80 and SWR1 chromatin remodeling complexes and in the NuA4 histone acetyltransferase complex. Here we show that arp4 (arp4S23AD159A) temperature-sensitive cells are defective in G2/M phase function. arp4 mutants are sensitive to the microtubule depolymering agent benomyl and arrest at G2/M phase at restrictive temperature. Arp4p is associated with centromeric and telomeric regions throughout cell cycle. Ino80p, Esa1p, and Swr1p, components of the INO80, NuA4, and SWR1 complexes, respectively, also associate with centromeres. The association of many kinetochore components including Cse4p, a component of the centromere nucleosome, Mtw1p, and Ctf3p is partially impaired in arp4 cells, suggesting that the G2/M arrest of arp4 mutant cells is due to a defect in formation of the chromosomal segregation apparatus. Keywords: ChIP-chip ⢠The goal of the experiment Genome-wide localization of Arp4 binding sites in Saccharomyces cerevisiae ⢠Experimental factors Distribution of Arp4 in WT in G2/M phase in the presence of nocodazole (Saccharomyces cerevisiae). ⢠Experimental design ChIP analysis: Hybridization data for ChIP fraction was compared with WCE (whole cell extract) fraction. Chromosome III, IV,V,VI S. cerevisiae: SC3456a520015F, P/N# 520015, affymetrix tiling array were used.
2010-06-11 | E-GEOD-7276 | biostudies-arrayexpress