bioRxiv Science⌕ Search

bioRxiv · 10.1101/2023.11.08.566223

Comprehensive IsomiR sequencing profile of human pancreatic islets and EndoC-βH1 beta-cells

Abstract

Aims/HypothesisMiRNAs play a crucial role in regulating the islet transcriptome, influencing beta cell functions and pathways. Emerging evidence suggests that during biogenesis a single miRNA locus can generate various sequences, known as isomiRNAs (isomiRs). However, a comprehensive profiling analysis of isomiRs in human pancreatic islets and beta cells is still lacking. This study aims to unveil the isomiRs expression profile in Laser Capture Microdissected (LCM) human pancreatic islets (HI) from non-diabetic donors and in the human beta cell line EndoC-{beta}H1, in order to shed light on novel molecular mechanisms governing beta cell function. MethodsRNA was extracted from LCM HI deriving from n=19 non-diabetic donors and from EndoC-{beta}H1 beta cells. Small RNA-seq was performed. Data were processed with the sRNAbench online pipeline for miRNAs/isomiRs quantification. Results were further validated using an external miRNA-seq database (isomiRdb). ResultsIn both HI and EndoC-{beta}H1, isomiRs accounted for a substantial proportion of total miRNA reads (HI: 59.4+/-1.9%; EndoC-{beta}H1: 43.8+/-0.6%). Among isomiRs, the most prevalent types were 3-end modifications, including trimming (HI=71.8+/-2.8%; EndoC-{beta}H1=55.8+/-1.0%) and extension (HI: 12.1+/-1.9%; EndoC-{beta}H1: 17.4+/-0.9%), followed by non-templated addition (HI: 9.8+/-0.9%; EndoC-{beta}H1: 14.0+/-1.2%). The analysis of the composition of the n=10 most expressed miRNAs highlighted a significant contribution of reads assigned to isomiRs. For instance, the most abundant miRNA, miR-375-3p, resulted from 59.7+/-2.4% of canonical and 40.3+/-2.4% of isomiRs in EndoC-{beta}H1 and from 45.3+/-2.0% of canonical and 54.7+/-2.0% of isomiR reads in HI. Interestingly, miR-7-5p, a beta cell-specific miRNA, was predominantly expressed as an isomiR both in EndoC-{beta}H1 (65.3+/-2.7%) and in HI (82.4+/-1.4%). To identify a reliable beta cell isomiR signature, common sequences detected in HI and EndoC-{beta}H1 were filtered based on their contribution to total miRNA expression, ultimately resulting in a set of 46 isomiRs. The expression of the isomiR signature in beta cells was further evaluated using an external database, isomiRdb, which contains small-RNA sequencing data from 99 different human cell types. This analysis revealed a significant enrichment of 11 out of the 46 isomiRs in beta cells compared to other cell types. The signature was functionally characterized through regression analysis with clinical and metabolic parameters related to beta cell function in non-diabetic individuals, demonstrating a significant negative correlation between basal insulin secretion and isomiR-411-5p, but not with its corresponding canonical miRNA. Conclusion/InterpretationThis study provides a comprehensive profile of isomiR expression in pancreatic islets and beta cells, highlighting the potential significance of isomiRs as novel regulators of beta cell function. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/566223v1_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@145f36borg.highwire.dtl.DTLVardef@1701433org.highwire.dtl.DTLVardef@13e5866org.highwire.dtl.DTLVardef@1dbe50_HPS_FORMAT_FIGEXP M_FIG C_FIG Research in ContextO_ST_ABSWhat is already know about this subject?C_ST_ABS- isomiRs are sequence variants of microRNAs (miRNAs) and may have distinct functional role respect to the canonical sequence. - isomiRs show cell/tissue specificity and are involved in multiple disease contexts. What is the key question?- What is the profile of isomiRs in human pancreatic islets (HI) and in beta cells? - Do isomiRs have a functional role in beta cells? What are the new findings?- IsomiRs represent a relevant fraction of total miRNAs in HI and beta cells. - 3end miRNA sequence modifications are the major fraction of isomiRs in beta cells. - A set of n=11 isomiRs, more expressed than their canonical miRNAs, are enriched in beta cells compared to the other human cell types. - Specific isomiRs are associated with beta cell glucose sensitivity and basal insulin secretion. How might this impact on clinical practice in the foreseeable future?- A comprehensive profile of isomiRs in beta cells may improve our understanding of molecular mechanisms driving beta cell function and dysfunction. - A highly detailed and granular view of miRNAs sequence variants and their expression levels may help in the design of novel therapeutic RNA-based strategies.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Auddino, S., Aiello, E., Toniolli, M., Grieco, G. E., Fignani, D., Licata, G., Bruttini, M., Mori, A., Berteramo, A. F., Pedace, E., Nigi, L., Formichi, C., Quero, G., Tondolo, V., Di Giuseppe, G., Soldovieri, L., Mari, A., Giaccari, A., Mezza, T., Dotta, F., Sebastiani, G.. 2023-11-08. Comprehensive IsomiR sequencing profile of human pancreatic islets and EndoC-βH1 beta-cells. https://doi.org/10.1101/2023.11.08.566223

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

LOca-1: A minimal calcium-activated arginyl-specific orthocaspase from the Loki's Castle hydrothermal vent field

Orthocaspases are prokaryotic homologs of metacaspases within the C14 family of cysteine proteases, yet their biochemical properties and cellular roles remain poorly understood. Here, we report the discovery and comprehensive characterization of LOca-1, a metagenome-derived orthocaspase from the Loki's Castle hydrothermal vent field. LOca-1 consists primarily of a single, conserved p20 catalytic domain and undergoes calcium-dependent activation through cleavage at a conserved arginine residue. Once activated, LOca-1 displays strict arginyl-specific proteolytic activity and strong selectivity for residues surrounding the cleavage site. The enzyme is both thermoactive and thermostable, exhibiting maximal activity at 65 {degrees}C and a melting temperature of approximately 72 {degrees}C. Structural modelling revealed conservation of the catalytic core relative to plant metacaspases despite substantial sequence divergence. To our knowledge, LOca-1 is only the second biochemically characterized orthocaspase and the first reported from a deep-sea hydrothermal vent environment. LOca-1 expands the known biochemical diversity of prokaryotic metacaspase homologs and provides insights into the properties of a minimal p20-domain orthocaspase. Together, our findings establish LOca-1 as a thermostable, calcium-activated arginyl-specific orthocaspase and provide a foundation for future studies of orthocaspase function in prokaryotes.

molecular biology↗

A TMEM175 Mutation Disrupts the Lysosomal-Mitochondrial Axis Causing Short QT Syndrome and Sudden Cardiac Death

Short QT Syndrome (SQTS) is a rare cardiac channelopathy characterized by abnormally short QTc intervals and increased sudden cardiac death (SCD) risk. Only 20-30% of SQTS cases have been linked to genetic mutations, typi-cally in surface membrane ion channels. We identified a novel lysosomal TMEM175 gene mutation (p.Arg377His) in 7 patients in a family with SQTS and SCD. Genetic analyses, including whole exome sequencing in the family and rare-variant burden testing in [~]118,000 UK Biobank participants, sug-gested an association between TMEM175 rare variants and QT interval short-ening. Functional studies in CRISPR-engineered mice and patient-specific induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) revealed that TMEM175R377H causes shortened QT intervals and hastened repolariza-tion, respectively, as well an increased arrhythmia susceptibility. Isolated TMEM175R377H cardiomyocytes showed action potential duration (APD) abbre-viation, confirmed in whole TMEM175R377H mouse hearts and patient-specific iPSC-CM monolayers. In silico and electron microscopy studies showed that TMEM175R377H disrupts lysosomal-mitochondrial interactions, leading to mito-chondrial dysfunction, as evidenced by the reduced maximal respiration and spare respiratory capacity, with reduced ATP production, IKATP activation, and APD shortening. This mutation represents the first non-sarcolemmal ion chan-nel defect associated with SQTS and high SCD risk, potentially expanding the genetic landscape of the disease.

molecular biology↗

Protecting host mitochondria with vitamin B3 preserves bioenergetics and thermogenesis during antibiotic treatment

Antibiotics that target bacterial translation can also impair mitochondrial function because mitochondria retain bacterial-like ribosomes. As antibiotic resistance continues to increase and the use of several broad-spectrum antibiotics has been limited by their mitochondrial toxicity, there is a growing need to understand their off-target effects in host physiology, and to identify strategies that can mitigate antibiotic-induced mitochondrial dysfunction. We demonstrate that antibiotic chloramphenicol (CA) induces a dose-dependent reduction in mitochondrial respiration and mitochondrial thermogenesis in Drosophila S2 cells, human HEK293T cells and in developing Drosophila larvae. In vivo, CA exposure triggers female-biased aberrant innate immune activation of hosts carrying naturally occurring mitochondrial rRNA variants. Metabolomic profiling revealed alterations in vitamin B3 metabolism in Drosophila during and following CA exposure. Among the vitamin B3 vitamers examined, nicotinamide (NAM) exhibited the strongest protective effect, mitigating the CA-induced impairments in mitochondrial respiration and thermogenesis, as well as aberrant immune activation. We identify mitochondrial thermogenesis as a previously unrecognized target of antibiotic-induced mitochondrial perturbation and a sensitive marker of mitochondrial stress. Furthermore, we demonstrate that co-supplementation of CA with NAM mitigates antibiotic-induced mitochondrial toxicity through evolutionarily conserved mitochondrial pathways. Finally, we establish Drosophila as a powerful model for investigating antibiotic-induced mitochondrial dysfunction and for developing therapeutic strategies to protect host mitochondria during antibiotic treatment.

molecular biology↗