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Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq

ABSTRACT: Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq

PROVIDER: PRJEB73634 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR12726930_1.fastq.gz	Fastqsanger.gz
	ERR12726930_2.fastq.gz	Fastqsanger.gz

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Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq

Project description:Single-cell RNA-sequencing (scRNAseq) is revolutionizing biomedicine, propelled by advances in methodology, ease of use, and cost reduction of library preparation. Over the past decade, there have been remarkable technical improvements in most aspects of single-cell transcriptomics. Yet, there has been little to no progress in advancing RNase inhibition despite that maintained RNA integrity is critical during cell collection, storage, and cDNA library generation. Here, we demonstrate that a synthetic thermostable RNase inhibitor yield single-cell libraries of equal or superior quality compared to ubiquitously used protein-based recombinant RNase inhibitors (RRIs). Importantly, the synthetic RNase inhibitor provide additional unique improvements in reproducibility and throughput, enable new experimental workflows including heat cycles, and can reduce the need for dry-ice transports. In summary, replacing RRIs represents a substantial advancement in the field of single-cell transcriptomics.

2024-07-29 | E-MTAB-13873 | biostudies-arrayexpress

Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq (Bulk RNA-seq libraries)

2024-07-26 | E-MTAB-13899 | biostudies-arrayexpress

Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq (Bulk RNA-seq libraries)

Project description:Introducing synthetic thermostable RNase inhibitors in single-cell RNA-seq (Bulk RNA-seq libraries)

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Synthetic lethal and resistance interactions with BET bromodomain inhibitors

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Structural determinants for tRNA selective cleavage by RNase 2/EDN

Project description:tRNA-derived fragments (tRFs) have emerged as key players of immunoregulation. Some RNase A superfamily members participate in the shaping of tRFs population. By comparing wild-type and knock-out macrophage cell lines our previous work (Lu L, et al. CMLS, 2022, 79: 209) revealed that RNase 2 can selectively cleave tRNAs. Here, we confirm the in vitro protein cleavage pattern by screening synthetic tRNAs, single-mutant variants and anticodon-loop DNA/RNA hairpins. By sequencing the tRFs products, we identified the cleavage selectivity by recombinant RNase 2 with base specificity at B1 (U/C) and B2 (A) sites, consistent with a previous cellular study. Knowledge of RNase 2 specific tRFs generation might guide new therapeutic approaches for infectious and immune-related diseases.

2024-05-29 | GSE250347 | GEO

Genome-wide alterations in yeast strains lacking RNase H1, RNase H2, or both RNase H1 and RNase H2

Project description:Two types of RNA:DNA associations can lead to genome instability: the formation of R-loops during transcription and the incorporation of ribonucleotide monophosphates (rNMPs) into DNA during replication. Both ribonuclease (RNase) H1 and RNase H2 degrade the RNA component of R-loops, whereas only RNase H2 can remove one or a few rNMPs from DNA. We performed high-resolution mapping of mitotic recombination events throughout the yeast genome in diploid strains of Saccharomyces cerevisiae lacking RNase H1 (rnh1Δ), RNase H2 (rnh201Δ), or both RNase H1 and RNase H2 (rnh1Δ rnh201Δ). We found little effect on recombination in the rnh1Δ strain, but elevated recombination in both the rnh201Δ and the double-mutant strains; levels of recombination in the double mutant were about 50% higher than in the rnh201 single-mutant strain. An rnh201Δ mutant that additionally contained a mutation that reduces rNMP incorporation by DNA polymerase ε (pol2-M644L) had a level of instability similar to that observed in the presence of wild-type Polε. This result suggests that the elevated recombination observed in the absence of only RNase H2 is primarily a consequence of R loops rather than misincorporated rNMPs.

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Synthetic lethal and resistance interactions with BET bromodomain inhibitors [Barcode_seq]

Project description:BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. The most prominent and consistent synergy was observed with CDK4/6 inhibitors and paclitaxel. We also uncovered functional similarities and differences between BBD proteins BRD2, BRD4, and BRD7, whereas deletion of BRD2 and BRD4 enhances sensitivity to BBDIs, BRD7 loss leads to resistance. Lastly, single cell RNA-seq and cellular barcoding analysis of BBDI responses in sensitive and resistant cell lines highlight heterogeneity among samples and demonstrate that BBDI resistance can be both pre-existing and acquired.

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