Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adaptive variation in mutagenesis driven by protein self-assembly

ABSTRACT: Adaptive variation in mutagenesis driven by protein self-assembly

PROVIDER: PRJNA1210016 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31986100_1.fastq.gz	Fastqsanger.gz
	SRR31986100_2.fastq.gz	Fastqsanger.gz
	SRR31986101_1.fastq.gz	Fastqsanger.gz
	SRR31986101_2.fastq.gz	Fastqsanger.gz
	SRR31986102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 178

Similar Datasets

Adaptive variation in mutagenesis driven by protein self-assembly

Project description:Mutations supply raw material for evolution. However, most are not adaptive. Thus, shifts in mutagenesis are typically transient. Nonetheless, modelling predicts that a heritable but revertible ‘mutagenesis switch’ would win in many selective landscapes. Here we report that prions formed by DNA repair proteins endow Saccharomyces cerevisiae with this capacity, sparking heritable variation in mutagenesis rates in evolving populations from the laboratory, nature, and the clinic. Self-templating transforms the functions and interactions of these DNA fidelity factors, enabling resilience to genotoxic stress and the emergence of drug resistance. In the fungal pathogen C. albicans, which diverged from S. cerevisiae ~300 million years ago, factors supporting prion inheritance promote the evolution of resistance to fluconazole, a mainline antifungal. Our findings suggest that protein self-assembly, a collective molecular behavior that is common among DNA replication and repair factors, can materialize epigenetic memory that tunes the balance of genome diversification and fidelity to expand adaptive opportunities.

2025-03-03 | GSE286868 | GEO

SYNCRIP is the Molecular Brake of APOBEC-driven Mutagenesis, Tumor Heterogeneity and Therapy Resistance

Project description:Intratumoral genetic heterogeneity and mutational burden have been suggested to be the fuel and the source of resistance for many molecularly targeted therapies throughout a multitude of cancers. Emerging evidence indicates that tumor cells could hijack the powerful mutagenesis machinery mediated by the DNA deaminase APOBEC family proteins to intensify mutagenesis, promote intratumoral heterogeneity, and foster therapy resistance through a cell-autonomous mechanism. However, this mechanism has yet to be characterized. Utilizing prostate cancer (PCa) as a relevant model, we have identified the Synaptotagmin Binding Cytoplasmic RNA Interacting Protein (SYNCRIP) as a molecular brake for APOBEC-driven mutagenesis, intratumoral heterogeneity, and resistance to Androgen Receptor (AR) targeted therapies. Through a multi-disciplinary approach integrating bulk and single cell RNA-Seq (scRNA-Seq), whole-genome exome-sequencing (WES), and CRISPR library screening, we identified eight mutated resistance driver genes and revealed unparalleled details of how these heterogeneously aberrant subclones fuel the evolution of AR therapy resistance. For the first time, these findings exposed a cell-autonomous mechanism activating APOBEC-driven mutagenesis, consequently fueling mutational burden, genetic heterogeneity, and therapy resistance, and suggested that APOBEC proteins could be the potential therapeutic targets for preventing or overcoming resistance in PCa.

2023-07-20 | GSE202321 | GEO

DNA mutagenesis driven by transcription factor competition with mismatch repair

Project description:DNA mutagenesis driven by transcription factor competition with mismatch repair

| PRJNA987713 | ENA

DNA mutagenesis driven by transcription factor competition with mismatch repair

Project description:DNA mutagenesis driven by transcription factor competition with mismatch repair

| PRJNA987708 | ENA

DNA mutagenesis driven by transcription factor competition with mismatch repair

Project description:DNA mutagenesis driven by transcription factor competition with mismatch repair

| PRJNA987711 | ENA

Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

Project description:Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

| PRJNA856647 | ENA

Deubiquitinating enzyme mutagenesis screens identify a USP43 driven HIF-1 transcriptional response

Project description:Deubiquitinating enzyme mutagenesis screens identify a USP43 driven HIF-1 transcriptional response

| PRJNA1061572 | ENA

Mechanism behind microalgal self-flocculation

Project description:Self-flocculation driven by gravity has shown as promising microalgal harvesting technology due to no requirement for additives and energies. However, the inherent unclear mechanism impedes its efficiency enhancement and commercial application. Current researches most only focus on the protein and carbohydrate content in extracellular polymeric substances (EPS), while further in-depth investigation is required on the detailed information of EPS components and their roles in self-flocculation.

2021-02-05 | PXD024007 |

RNA sequence to structure analysis from comprehensive pairwise mutagenesis of multiple self-cleaving ribozymes

Project description:RNA sequence to structure analysis from comprehensive pairwise mutagenesis of multiple self-cleaving ribozymes

| PRJEB52899 | ENA

Deubiquitinating enzyme mutagenesis screens identify a USP43 driven HIF-1 transcriptional response [CRISPR]

Project description:Deubiquitinating enzyme mutagenesis screens identify a USP43 driven HIF-1 transcriptional response [CRISPR]

| PRJNA1061568 | ENA