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Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5

ABSTRACT: Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5

PROVIDER: PRJNA1139208 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29932348.fastq.gz	Fastqsanger.gz
	SRR29932349.fastq.gz	Fastqsanger.gz
	SRR29932350.fastq.gz	Fastqsanger.gz
	SRR29932351.fastq.gz	Fastqsanger.gz
	SRR29932352.fastq.gz	Fastqsanger.gz

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Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5 [ChIP-Seq]

Project description:Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5 [ChIP-Seq]

| PRJNA1140126 | ENA

Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5

Project description:MicroRNAs (miRNAs) are small non-coding RNAs that play crucial roles in post-transcriptional gene regulation. Poly(A) RNA polymerase D5 (PAPD5) catalyzes the addition of adenosine to the 3′ end of miRNAs. In this study, we demonstrated that the Yin Yang 1 protein, a transcriptional repressor of PAPD5, was recruited to both RNA foci and protein aggregates, resulting in an upregulation of PAPD5 expression in Huntington’s disease (HD). Additionally, we identified a subset of PAPD5-regulated miRNAs with increased adenylation and reduced expression in our disease model. We focused on miR-7-5p and found that its reduction caused the activation of the TAB2-mediated TAK1–MKK4–JNK pro-apoptotic pathway. This pathway was also activated in induced pluripotent stem cell-derived striatal neurons and post-mortem striatal tissues isolated from HD patients. In addition, we discovered that a small molecule PAPD5 inhibitor, BCH001, could mitigate cell death and neurodegeneration in our disease models. This study highlights the importance of PAPD5-mediated miRNA dysfunction in HD pathogenesis and suggests a potential therapeutic direction for the disease.

2024-08-01 | GSE272903 | GEO

Mutant huntingtin induces neuronal apoptosis via derepressing the non-canonical poly(A) polymerase PAPD5 [ChIP-Seq]

2024-08-01 | GSE273082 | GEO

PAPD5, a noncanonical poly(A) polymerase with an unusual RNA-binding motif [PAR-CLIP]

2012-04-03 | GSE36987 | GEO

PAPD5, a noncanonical poly(A) polymerase with an unusual RNA-binding motif [PAR-CLIP]

Project description:PAPD5 is one of the seven members of non-canonical poly(A) polymerases in human cells. There are previous reports about polyadenylation dependent degradation of pre-ribosomal RNAs and uridylation dependent degradation of histone mRNAs in vivo. In this study, we observed polyadenylation but not polyuridylation activity of PAPD5 with in vitro assays. We aimed to get genome-wide targets of PAPD5 and used PAR-CLIP and deep sequencing for this purpose. Recombinant version of PAPD5 is expressed in HEK293 human cell lines and its genome wide targets are obtained with PAR-CLIP and deep sequencing as two replicate experiments. The short reads in the deep sequencing libraries of PAPD5 replicates and an unrelated protein to polymerization from a previous study, IGF2BP1, are aligned to the hg18 human genome assembly. The biological variance of the read counts in overlapping 100-nucleotide-long-windows is estimated between the PAPD5 replicates and further used in the differential expression estimations between the 100-nucleotide windows in PAPD5 replicates and IGF2BP1. The top differentially expressed windows in PAPD5 and IGF2BP1 are further annotated using gene and repeat tracks from UCSC.

2012-04-02 | E-GEOD-36987 | biostudies-arrayexpress

The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis

Project description:The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis

| PRJNA1029581 | ENA

The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis [RIP]

Project description:The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis [RIP]

| PRJNA1029586 | ENA

The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis [ADAR_APOBEC]

Project description:The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis [ADAR_APOBEC]

| PRJNA1029583 | ENA

RNA-seq of allelic series of mouse Huntingtin knock-in cells

Project description:In order to study the role of Poly-Q length of Huntingtin we performed RNA-seq on knock-in cells bearing Huntingtin with 0Q, 2Q, 4Q, or 7Q (3 biological replicates per cell line) at the rosette (day 8) and neuronal (day 28) stage of differentiation. Two differential expression analyses were performed: static pairwise comparison among all the cell lines for each time points, and dynamic pairwise comparison between time points for each cell line.

2022-04-26 | E-MTAB-9378 | biostudies-arrayexpress

mTOR- and LARP1-dependent regulation of TOP mRNA poly(A) tail and ribosome loading [polysome fractionation]

Project description:Translation of TOP mRNAs encoding protein synthesis machinery is strictly regulated by an amino acid sensing mTOR pathway. However, its regulatory mechanism remains elusive. Here, we demonstrate that TOP mRNA translation positively correlates with its poly(A) tail length under mTOR active/amino acid-rich condition, suggesting that TOP mRNAs are post-transcriptionally controlled by poly(A) tail length regulation. Consistent with this, tail length of TOP mRNAs dynamically fluctuates in response to amino acid availability. Poly(A) tail shortens under mTOR active/ amino acid-rich condition, whereas the long-tailed TOP mRNAs accumulate under mTOR inactive/amino acid-starved (AAS) condition. An RNA-binding protein LARP1 that specifically binds to TOP mRNAs is indispensable for the process. We also show that LARP1 interacts with non-canonical poly(A) polymerases, PAPD4, PAPD5 and PAPD7 and induces post-transcriptional polyadenylation of the target when tethered to the mRNA. Our findings illustrate that LARP1 contributes to the selective accumulation of TOP mRNAs with long poly(A) tail under AAS, resulting in accelerated ribosomal loading onto TOP mRNAs for the resumption of translation after AAS.

2022-09-22 | GSE145744 | GEO

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