Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10692929_1.fastq.gz | Fastqsanger.gz | |||
| SRR10692929_2.fastq.gz | Fastqsanger.gz | |||
| SRR10692930_1.fastq.gz | Fastqsanger.gz | |||
| SRR10692930_2.fastq.gz | Fastqsanger.gz | |||
| SRR10692931_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Evaluate the transcriptional profile of genes involved in fungus-host interactions using RNA sequencing Methods: T. rubrum and HaCat cells line were co-cultured in RPMI medium supplemented with 5% of fetal bovine serum and were incubated for 24 h at 37ºC in a humidified atmosphere containing 5% CO2 , followed RNA by extraction of both organisms, libraries construction and sequence. Results: Our data demonstrated the induction of specific genes that may improve the assimilation of nutrients and fungal survival in the host and genes encoding keratinolytic proteases that are important for T. rubrum virulence during infection. In HaCat cell lines it were induced genes encoding antimicrobial activity , cell migration and epithelial barrier repair. Futhermore, the genes KRT1 and FLG involved in epithelial barrier integrity were repressed Conclusions: This mixed transcriptome analysis showed the modulation of important genes involved in the mechanism of T. rubrum infection and in the defense and maintenance of cell homeostasis of keratinocytes, which could represent potential antifungal targets for new therapeutic approaches to the treatment of dermatophytoses
2018-07-30 | GSE110073 | GEO
Project description:We complemented our genomic investigations with keratinolytic activity and cellular metabolism reconsctruction, yielding a more comprehensive view of the degradation process.
| PRJEB38982 | ENA
Project description:Experience-dependent gene transcription is required for nervous system development and function. However, the DNA regulatory elements that control this program of gene expression are not well defined. Here we characterize the enhancers that function across the genome to mediate activity-dependent transcription in neurons. While ~12,000 putative activity-regulated enhancer sequences have previously been identified that are enriched for H3K4me1 and the histone acetyltransferase CBP, we find that this chromatin signature is not sufficient to distinguish which of these regulatory sequences are actively engaged in promoting activity-dependent transcription. We show here that a subset of H3K4me1/CBP positive enhancers that is enriched for H3K27 acetylation (H3K27ac) in vivo, and shows increased H3K27ac upon membrane depolarization of cortical neurons, function to regulate activity-dependent transcription. The function of many of these activity-regulated enhancers appears to be dependent on the binding of FOS, a protein that had previously been thought to interact primarily with the promoters of activity-regulated genes. Furthermore, many of these target genes in cortical neurons encode neuron specific proteins that regulate synaptic development and function. These findings suggest that FOS functions at enhancers to control activity-dependent gene programs that are critical for nervous system function, and provide a resource of activity-dependent enhancers that may give insight into genetic variation that contributes to brain development and disease. Genome-wide maps of H3K27ac and AP1 transcription factors (CFOS, FOSB, JUNB) before and after neuronal activity in mouse cortical neurons.
2014-09-07 | E-GEOD-60192 | biostudies-arrayexpress
Project description:Despite correlations between histone methyltransferase (HMT) activity and gene regulation, direct evidence that HMT activity is responsible for gene activation is sparse. We address the role of the HMT activity for MLL1, a histone H3 lysine 4 (H3K4) methyltransferase critical for maintaining hematopoietic stem cells (HSCs). Here we show that the SET domain and thus HMT activity of MLL1 is dispensable for maintaining HSCs and for supporting leukemogenesis driven by the MLL-AF9 fusion oncoprotein. Upon Mll1 deletion, histone H4 lysine 16 (H4K16) acetylation was selectively depleted at MLL1 target genes in conjunction with reduced transcription. Surprisingly, inhibition of SIRT1 was sufficient to prevent the loss of H4K16 acetylation and the reduction in MLL1 target gene expression. Thus, recruited MOF activity, and not the intrinsic HMT activity of MLL1, is central for the maintenance of HSC target genes. In addition, this work reveals a role for SIRT1 in opposing MLL1 function. 11 Samples, 5 controls and 5 KOs with antibodies H3K4me1, H3K4me3, and H3K27Ac. One input Sample.
2014-04-03 | E-GEOD-56456 | biostudies-arrayexpress