Oryza sativa Japonica Group
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-50777
PROVIDER: PRJNA218883 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR976335.fastq.gz | Fastqsanger.gz | |||
| SRR976336.fastq.gz | Fastqsanger.gz | |||
| SRR976337.fastq.gz | Fastqsanger.gz | |||
| SRR976338.fastq.gz | Fastqsanger.gz | |||
| SRR976339.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
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Project description:The apicomplexan parasite Cryptosporidium is a leading global cause of severe diarrheal disease and an important contributor to early childhood mortality. Currently there are no fully effective treatments or vaccines available. Transmission of the disease occurs through ingestion of oocysts, through direct contact or contaminated water or food. Oocysts are meiotic spores and the product of parasite sex. Cryptosporidium has a single host lifecycle where both asexual and sexual processes unfold in the intestine of infected hosts. Here we use the new-found ability to genetically engineer Cryptosporidium to make life cycle progression and parasite sex tractable. We derive reporter strains to follow parasite development in culture and infected mice and define the genes that orchestrate sex and oocyst formation through mRNA sequencing of sorted cells. After two days, parasites in cell culture show pronounced sexualization, but productive fertilization does not occur and infection falters. In contrast in infected mice, male gametes successfully fertilize females, leading to meiotic division and sporulation. To rigorously test for fertilization, we devised a two-component genetic crossing assay employing a Cre recombinase activated reporter. Our findings suggest obligate developmental progression towards sex in Cryptosporidium, which has important implications for the treatment and prevention of the infection.
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Project description:For animals, epigenetic modifications can be globally or partially inherited from gametes after fertilization, but the mechanism underlying how the inherited epigenetic signatures affect transcriptional regulation during zygotic genome activation (ZGA) remains poorly understood. Here, we performed genome-wide profiling of chromatin accessibility during zebrafish ZGA, which is closely related to zygotic transcriptional regulation. The locations of the accessible chromatin at promoters were precisely primed by the enrichment of unmethylated CpGs that were fully inherited from gametes. On the other hand, distal regions with high methylation levels that were inherited from the sperm facilitated the binding of DNA methylation-preferred transcription factors, such as pou5f3 and nanog, which contributed to the establishment of accessible chromatin at these loci. Our results demonstrate a model whereby inherited DNA methylation signatures from gametes prime the establishment of accessible chromatin during zebrafish ZGA through two distinct mechanisms.
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