Differential gene expression of gene during media induced aggregation
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ABSTRACT:
PROVIDER: PRJNA983706 | ENA |
REPOSITORIES: ENA
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Project description:This study aimed to characterise the transcriptional response of two strains of Candida auris (UACa11 and UACa20) during media-induced aggregation due to differences in phenotype. RNA was isolated from each strain under both aggregating and non-aggregating culture conditions.
2024-03-01 | GSE234899 | GEO
Project description:Protein aggregation is a hallmark of many neurodegenerative diseases. In order to cope with misfolding and aggregation, cells have evolved an elaborate network of molecular chaperones, composed of different families. But while chaperoning mechanisms for different families are well established, functional and regulatory diversification within chaperone families is still largely a mystery. Here we decided to explore chaperone functional diversity, through the lens of pathological aggregation. We revealed that different naturally-occurring isoforms of DNAJ chaperones showed differential effects on different types of aggregates. We performed a chaperone screen for modulators of two neurodegeneration-related aggregating proteins, the Huntington’s disease-related HTT-polyQ, and the ALS-related mutant FUS (mutFUS). The screen identified known modulators of HTT-polyQ aggregation, confirming the validity of our approach. Surprisingly, modulators of mutFUS aggregation were completely different than those of HTT-polyQ. Interestingly, different naturally-occurring isoforms of DNAJ chaperones had opposing effects on HTT-polyQ vs. mutFUS aggregation. We identified a complex of the full length (FL) DNAJB14 and DNAJB12 isoforms which substantially alleviated mutFUS aggregation, in an HSP70-dependent manner. Their naturally occurring short isoforms were unable to form the complex, nor to interact with HSP70, and lost their ability to reduce mutFUS aggregation. In contrast, the short isoform of DNAJB12 significantly alleviated HTT-polyQ aggregation, while DNAJB12-FL aggravated HTT-polyQ aggregation. Finally, we demonstrated that full-length DNAJB14 ameliorated mutFUS aggregation compared to DNAJB14-short in primary neurons. Together, our data unraveled distinct molecular properties required for aggregation protection in different neurodegenerative diseases, and revealed a new layer of complexity of the chaperone network elicited by naturally occurring J-protein isoforms, highlighting functional diversity among the DNAJ family.
2021-12-07 | GSE165317 | GEO
Project description:In this study the generic impact of protein aggregation (aggregation of proteins not associated with neurodegenerative disease) on gene expression in cultured cells was investigated by DNA microarray technology. The survey of gene expression showed that the Hsp40, Hsp70 and Hsp105 genes, all of which have documented aggregation suppression activity, were up-regulated. Unexpectedly, the survey also showed increased expression of the MEK5 gene with concomitant silencing of the MEK3 gene. The expression pattern of MEK5 at the mRNA and protein levels aligns with the kinetics of aggregate formation and dissolution. Cell viability was unaffected by protein aggregates. These findings are of particular importance for chronic neurodegenerative diseases where the intraneuronal accumulation of aggregate-prone proteins are a major characteristic of the diseases. The identification of changes in MEK5 gene expression have been observed in Alzheimer-related diseases which provides new diagnostic and therapeutic avenues in these diseases. The molecular neuropathological findings would not have occurred without the generic microarray analyses.
2005-07-20 | E-MEXP-389 | biostudies-arrayexpress
Project description:Investigation of very early events required for initiating differentiation of pluripotent embryonal carcinoma cells - the effect of cell aggregation on gene expression. Keywords: cell aggregation
2006-01-24 | GSE4085 | GEO
Project description:Saccharomyces cerevisiae colonies were grown for 2 days on synthetic minimal media with 1% glucose, with and without 400uM lysine (5 colonies/biological replicates each). Whole colonies were then used for proteome profiling by SWATH-MS for differential gene expression analysis. A number of genes were identified that respond to lysine supplementation, most notably genes involved in lysine biosynthesis.
2023-02-13 | PXD030702 | Pride
Project description:Our goal was to better understand the genes and pathways implicated during arterial media aging. We therefore compared the gene expression profile of human mammary artery media between Young (<60, 8 patients) and old (>75, 7 patients) patients. The microarray data, generated using the Illumina sentrix Ref8-V2 platform, was normalized and analyzed using the IlluminaGUI package (Eggle and Schultze, 2007).
2010-12-07 | GSE16487 | GEO
Project description:Protein misfolding and aggregation deregulate the proteostasis network and are hallmarks of cell degeneration processes associated with aging and human diseases. But how proteome aggregation causes cell degeneration remains controversial due to the lack of suitable methods for controlling proteome aggregation at the cellular and organismal levels. To overcome this limitation, we have generated zebrafish embryos that exhibit protein aggregation due to misincorporation of Serine (Ser) at non-cognate protein sites on a proteome wide scale. These mistranslating embryos display up regulation of the unfolded protein response (UPR) and the ubiquitin proteasome pathway (UPP), increased protein ubiquitination and down-regulation of protein biosynthesis. Proteome damage also induces major disruption of the mitochondrial network, accompanied by mitochondrial and nuclear DNA damage and accumulation of reactive oxygen species (ROS). Taken together, our data highlight important roles of gene translational accuracy in the maintenance of ER homeostasis, DNA damage, mitochondrial function and oxidative stress. We postulate that protein biosynthesis errors (PBE) contribute to proteome aggregation and are a main cause of mitochondrial disruption.
2018-01-29 | GSE50090 | GEO
Project description:PKM2 aggregation drives metabolism reprograming during aging process
| PRJNA1118725 | ENA
Project description:To validate that the aggregation pattern identifies a pro-tumoral Mφ subset in HCC, we have employed microarray expression profiling as a discovery platform to identify the molecular and functional implications of Mφ spatial distribution in HCC. Gene ontology (GO) and gene-set enrichment analyses (GSEA) revealed that tissues rich in aggregated Mφs significantly upregulated tissue remodeling pathways and “M2” Mφ-associated genes, while pro-inflammatory “M1” gene sets were more pronounced in HCCs with predominantly scattered Mφs. These results indicate that Mφ aggregation signifies a transition to a multifaceted, pro-tumoral phenotype, highlighting the intricate relationship between spatial distribution and function of Mφs in the tumor milieu.
2024-09-08 | GSE276428 | GEO
Project description:Differential expression gene signature
| PRJNA971197 | ENA