Ontology highlight
ABSTRACT:
PROVIDER: PRJEB36403 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3888660_1.fastq.gz | Fastqsanger.gz | |||
| ERR3888660_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:The lysosomal function is down-regulated in the white prepupal fat body, resulting in the enlargement of lysosomes in the tissue. The enlargement is blocked by the forced activation of lysosomes by the overexpression of mitf, a sole homolog of the MiTF/TFE family transcription factors. Thus, it is possible to speculate that mitf participates in the down-regulation of lysosomes in the fat body. To test this possibility, we performed a comparative mRNA-seq of (1) wild-type white prepupal fat body, (2) mitf overexpressed white prepupal fat body, and (3) wild-type third instar larval fat body. First, a comparison of (1) and (2) showed that the overexpression of mitf upregulated transcription of most of the lysosome-related genes in the fat body, consistent with previous studies. Next, a comparison of (1) and (3) indicated that the transcription level of several lysosome-related genes was decreased in (1) compared to (3). However, most of the genes regulated by Mitf were not transcriptionally affected. These results suggest that mitf is dispensable for the downregulation of lysosomes in the white prepupal fat body.
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Project description:There is growing evidence that genomic DNA sequence changes occur in individual somatic cells during the lifetime of an individual and accumulation of these changes may influence aging and disease. In light of this, and contradicting reports regarding discordant copy number profiles between MZ twins(BARANZINI et al. 2010; BRUDER et al. 2008), we set out to identify de novo somatic copy number mutations in DNA from blood for MZ twin pairs of Mexican American descent who were participants of the San Antonio Family Heart Study (SAFHS) or San Antonio Family Diabetes/Gallbladder study (SAFDGS). By applying circular binary segmentation (CBS) to B-allele ratio differences we determined that the 3 MZ twin pairs in this study had concordant copy number profiles. We also detected 2 de novo germ-line CNVs in 2 MZ twin pairs from the SAFHS. This study includes data for 4 monozygotic (MZ) twin pairs, and both parents of 2 of these MZ twin pairs. The purpose of this study was to compare concordance of copy number profiles between MZ twins.
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Project description:The biosynthesis of androgen from cholesterol in testis is well understood, however, how cancer cells gauge dwindling androgen to dexterously initiate its de novo synthesis remained elusive. We uncovered that sterol regulatory element-binding protein 1 (SREBP1) and its switch to hitherto unknown dual-phosphorylated form (pY673/951-SREBP1), acts as an androgen sensor. Androgen deficiency promoted SREBP1 dual-phosphorylation, causing its dissociation from androgen receptor (AR) in its androgen-unbound state, followed by nuclear translocation. SREBP1 recruited KAT2A/GCN5 and deposited novel epigenetic marks, histone H2A Lys130-acetylation (H2A-K130ac) in SREBF1, reigniting de novo lipogenesis & steroidogenesis. Tumor-derived androgen retained SREBP1 in cytosol, promoting T cell exhaustion, reflected in elevated PD-1 and Tim3. Reversal of H2A-K130ac or pY-SREBP1 sensitized castration-resistant prostate cancer (CRPC) resistant to androgen synthesis inhibitor, Abiraterone. Further, nuclear SREBP1 and H2A-K130ac levels were significantly increased and directly correlated with late stage prostate cancer patients. Global lipidomics analysis revealed a distinct lipid signature in androgen-deprived CRPCs, resembling the lipid profile of prostate cancers of African-American (AA) men. Overall, self-perpetuating pY-SREBP1/H2A-K130ac signaling explains sex bias in cancers and reveal a novel therapeutic vulnerability wherein synchronous inhibition of GCN5 and Tyr-kinases could overcome drug-resistant disease, benefiting AA men with aggressive prostate cancer.
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