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Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [miRNA-seq]

ABSTRACT: Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [miRNA-seq]

PROVIDER: PRJNA720704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17075200.fastq.gz	Fastqsanger.gz
	SRR17075201.fastq.gz	Fastqsanger.gz
	SRR17075202.fastq.gz	Fastqsanger.gz
	SRR17075203.fastq.gz	Fastqsanger.gz
	SRR17075204.fastq.gz	Fastqsanger.gz

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Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [Ribo-seq]

Project description:The C.elegans translatomes of single-nt let-7a 3' non-seed mutants (U13A / U18A). In order to identified gene perturbance caused by disrupting 3' non-seed pairing of let-7a, we examined the global gene expression at tranlational levels of L4 whole animals by ribosome profiling. We found that let-7a U13A mutation results in overexpression135/351 Note for let-7a U13A mutation, lin-41(ma480) was used in the background to filter out downstream regulation related to the lin-41 pathway.

2021-04-09 | GSE171726 | GEO

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [RNA-seq]

Project description:The C.elegans transcriptomes of single-nt let-7a 3' non-seed mutants (U13A / U18A). In order to identified gene perturbance and determine the post-transcriptional regulation mechanism caused by disrupting 3' non-seed pairing of let-7a, we examined the global gene expression by RNAseq in addition to ribosome profiling of L4 whole animals. To include the deadenylated but temperally stable mRNA in the enrichment, we used a RNase H based ribosomal RNA depletion with antisense oligos specifically designed for C.elegans to enrich mRNA (PMID: 33005886). lin-41(ma480) was used in the background to filter out downstream regulation related to the lin-41 pathway.

2021-04-09 | GSE171733 | GEO

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA

Project description:Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA

| PRJNA720701 | ENA

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [miRNA-seq]

Project description:Small RNA sequencing of all the let-7a single-nucleotide mutants to confirm the expression of the mutant miRNAs.We found that the abundance of the mutated let-7a miRNA in each mutant was similar to that of the native let-7a in WT, with a variance (<10%) that we judge not sufficient to cause lf phenotypes by reduced expression (Fig. 3B). Note that the strains with mutations at g11-g16 also contained a WT let-7 allele on a genetic balancer umnIs25(mnDp1), hence both WT and mutant let-7a were expressed.

2021-12-06 | GSE171747 | GEO

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [Ribo-seq]

Project description:Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [Ribo-seq]

| PRJNA720671 | ENA

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [RNA-seq]

Project description:Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA [RNA-seq]

| PRJNA720677 | ENA

Critical contribution of 3' non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA.

Project description:Base pairing of the seed region (g2-g8) is essential for microRNA targeting; however, the in vivo function of the 3' non-seed region (g9-g22) is less well understood. Here, we report a systematic investigation of the in vivo roles of 3' non-seed nucleotides in microRNA let-7a, whose entire g9-g22 region is conserved among bilaterians. We find that the 3' non-seed sequence functionally distinguishes let-7a from its family paralogs. The complete pairing of g11-g16 is essential for let-7a to fully repress multiple key targets, including evolutionarily conserved lin-41, daf-12, and hbl-1. Nucleotides at g17-g22 are less critical but may compensate for mismatches in the g11-g16 region. Interestingly, a certain minimal complementarity to let-7a 3' non-seed sequence can be required even for sites with perfect seed pairing. These results provide evidence that the specific configurations of both seed and 3' non-seed base pairing can critically influence microRNA-mediated gene regulation in vivo.

| S-EPMC9161110 | biostudies-literature

Critical contribution of 3’ non-seed base pairing to the in vivo function of the evolutionarily conserved let-7a microRNA

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-09 | GSE171748 | GEO

Functional microRNA targeting without seed pairing

Project description:Functional microRNA targeting without seed pairing

| PRJNA1228674 | ENA

miRNA let-7a-3 overexpression in lung cancer cell line A549

Project description:MicroRNAs (miRNAs) are small non-coding RNAs that repress their target mRNAs by complementary base pairing and induction of the RNAi pathway. It has been shown that miRNA expression can be regulated by DNA methylation and it has been suggested that altered miRNA gene methylation might contribute to human tumorigenesis. In this study, we show that the human let-7a-3 gene on chromosome 22q13.31 is associated with a CpG island. Let-7a-3 belongs to the archetypal let-7 miRNA gene family DNA methylation and was found to be methylated by the DNA methyltransferases DNMT1 and DNMT3B. The gene was heavily methylated in normal human tissues, but hypomethylated in some human lung adenocarcinomas. Let-7a-3 hypomethylation facilitated epigenetic reactivation of the gene and elevated expression of let-7a-3 in a human lung cancer cell line resulted in enhanced tumor phenotypes and oncogenic changes in transcription profiles. Keywords: genetic modification

2007-01-15 | GSE6474 | GEO

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