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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE171748 | GEO | 2021/04/09

REPOSITORIES: GEO

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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 [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 [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 [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

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 [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 [miRNA-seq]

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

| PRJNA720704 | 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

Podocyte GSK3 is an evolutionarily conserved critical regulator of kidney function.

Project description:Albuminuria affects millions of people, and is an independent risk factor for kidney failure, cardiovascular morbidity and death. The key cell that prevents albuminuria is the terminally differentiated glomerular podocyte. Here we report the evolutionary importance of the enzyme Glycogen Synthase Kinase 3 (GSK3) for maintaining podocyte function in mice and the equivalent nephrocyte cell in Drosophila. Developmental deletion of both GSK3 isoforms (? and ?) in murine podocytes causes late neonatal death associated with massive albuminuria and renal failure. Similarly, silencing GSK3 in nephrocytes is developmentally lethal for this cell. Mature genetic or pharmacological podocyte/nephrocyte GSK3 inhibition is also detrimental; producing albuminuric kidney disease in mice and nephrocyte depletion in Drosophila. Mechanistically, GSK3 loss causes differentiated podocytes to re-enter the cell cycle and undergo mitotic catastrophe, modulated via the Hippo pathway but independent of Wnt-?-catenin. This work clearly identifies GSK3 as a critical regulator of podocyte and hence kidney function.

| S-EPMC6345761 | biostudies-literature

Evolutionarily conserved histone methylation dynamics during seed life-cycle transitions.

Project description:Plants have a remarkable ability to react to seasonal changes by synchronizing life-cycle transitions with environmental conditions. We addressed the question of how transcriptional re-programming occurs in response to an environmental cue that triggers the major life cycle transition from seed dormancy to germination and seedling growth. We elucidated an important mechanistic aspect of this process by following the chromatin dynamics of key regulatory genes with a focus on the two antagonistic marks, H3K4me3 and H3K27me3. Histone methylation patterns of major dormancy regulators changed during the transition to germination and seedling growth. We observed a switch from H3K4me3 and high transcription levels to silencing by the repressive H3K27me3 mark when dormancy was broken through exposure to moist chilling, underscoring that a functional PRC2 complex is necessary for this transition. Moreover, this reciprocal regulation by H3K4me3 and H3K27me3 is evolutionarily conserved from gymnosperms to angiosperms.

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