Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Ccr4-Not complex monitors the translating ribosome for codon optimality

ABSTRACT: The Ccr4-Not complex monitors the translating ribosome for codon optimality

PROVIDER: PRJNA603124 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10963471.fastq.gz	Fastqsanger.gz
	SRR10963472.fastq.gz	Fastqsanger.gz
	SRR10963473.fastq.gz	Fastqsanger.gz
	SRR10963474.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

The Ccr4-Not complex monitors the translating ribosome for codon optimality

Project description:The Ccr4-Not complex monitors the translating ribosome for codon optimality

| PRJNA543493 | ENA

The Ccr4-Not complex monitors the translating ribosome for codon optimality

Project description:Control of messenger RNA (mRNA) decay rate is intimately connected to translation elongation, but the spatial coordination of these events is poorly understood. The Ccr4-Not complex initiates mRNA decay through deadenylation and activation of decapping. We used a combination of cryo–electron microscopy, ribosome profiling, and mRNA stability assays to examine the recruitment of Ccr4-Not to the ribosome via specific interaction of the Not5 subunit with the ribosomal E-site in Saccharomyces cerevisiae. This interaction occurred when the ribosome lacked accommodated A-site transfer RNA, indicative of low codon optimality. Loss of the interaction resulted in the inability of the mRNA degradation machinery to sense codon optimality. Our findings elucidate a physical link between the Ccr4-Not complex and the ribosome and provide mechanistic insight into the coupling of decoding efficiency with mRNA stability.

2020-04-16 | GSE131408 | GEO

The Ccr4-Not complex monitors the translating ribosome for codon optimality

2020-04-16 | GSE144250 | GEO

The Ccr4-Not complex monitors the translating ribosome for codon optimality.

Project description:Control of messenger RNA (mRNA) decay rate is intimately connected to translation elongation, but the spatial coordination of these events is poorly understood. The Ccr4-Not complex initiates mRNA decay through deadenylation and activation of decapping. We used a combination of cryo-electron microscopy, ribosome profiling, and mRNA stability assays to examine the recruitment of Ccr4-Not to the ribosome via specific interaction of the Not5 subunit with the ribosomal E-site in Saccharomyces cerevisiae This interaction occurred when the ribosome lacked accommodated A-site transfer RNA, indicative of low codon optimality. Loss of the interaction resulted in the inability of the mRNA degradation machinery to sense codon optimality. Our findings elucidate a physical link between the Ccr4-Not complex and the ribosome and provide mechanistic insight into the coupling of decoding efficiency with mRNA stability.

| S-EPMC8663607 | biostudies-literature

Mutability and hypermutation antagonize immunoglobulin codon optimality; Analysis of human MLN B cells.

Project description:The main objective of this study was to analyze codon optimality in relation to somatic hypermutation in natural V(D)J repertoires.

2024-10-24 | GSE260944 | GEO

Mutability and hypermutation antagonize immunoglobulin codon optimality; Analysis of human tonsil B cells.

Project description:The main objective of this study was to analyze codon optimality in relation to somatic hypermutation in natural V(D)J repertoires.

2024-10-24 | GSE260943 | GEO

Mutability and hypermutation antagonize immunoglobulin codon optimality; Analysis of mouse splenic B cells.

Project description:The main objective of this study was to analyze codon optimality in relation to somatic hypermutation in natural V(D)J repertoires.

2024-10-24 | GSE260942 | GEO

Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes (Ribo-seq)

Project description:The CCR4-NOT complex is a major regulator of eukaryotic messenger RNA (mRNA) stability. Slow decoding during translation promotes association of CCR4-NOT with ribosomes, accelerating mRNA degradation. We applied selective ribosome profiling to further investigate the determinants of CCR4-NOT recruitment to ribosomes in mammalian cells. This revealed that specific arginine codons in the P-site are strong signals for ribosomal recruitment of human CNOT3, a CCR4-NOT subunit. Cryo–electron microscopy and transfer RNA (tRNA) mutagenesis demonstrated that the D-arms of select arginine tRNAs interact with CNOT3 and promote its recruitment whereas other tRNA D-arms sterically clash with CNOT3. These effects link codon content to mRNA stability. Thus, in addition to their canonical decoding function, tRNAs directly engage regulatory complexes during translation, a mechanism we term P-site tRNA-mediated mRNA decay.

2024-11-21 | GSE268324 | GEO

Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes (SLAM-Seq)

2024-11-21 | GSE268322 | GEO

Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human tonsil B cells.

Project description:Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human tonsil B cells.

| PRJNA1084084 | ENA