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MicroRNAs01:22

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
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Targeted blocking of gene splicing can dysregulate intron-embedded primary microRNAs.

Md Hasan Ali1, Athul R Ramesh1, Naveen Nedunchezhian1

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Antisense oligonucleotides (ASOs) targeting intronic noncoding RNAs (ncRNAs) can unexpectedly increase microRNA expression, impacting neuronal development. This study reveals how ASOs affect intronic ncRNAs and suggests using these effects to identify microRNA roles.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Antisense oligonucleotides (ASOs) are investigated for therapeutic potential, but their impact on intronic noncoding RNAs (ncRNAs) is not fully understood.
  • Intronic ncRNAs, including microRNAs, play critical roles in gene regulation and cellular function.
  • Understanding ASO interactions with intronic ncRNAs is vital for successful clinical applications.

Purpose of the Study:

  • To investigate the effects of ASO-mediated targeting of intronic ncRNAs on gene expression and function.
  • To determine if ASO targeting of intronic regions influences the expression and activity of embedded microRNAs.
  • To explore the consequences of altered intronic ncRNA expression on neuronal development, specifically pituitary axonal morphogenesis in zebrafish.

Main Methods:

  • Utilized antisense oligonucleotides (ASOs) targeting specific splice sites and translation start sites of the slit3 gene in zebrafish.
  • Analyzed gene expression, splicing patterns, and microRNA levels (mir-218a-1) using molecular techniques.
  • Investigated phenotypes in mir-218a-1 knockout mutants and through mir-218a-1 mimic injection.
  • Assessed the role of nonsense-mediated decay (NMD) in regulating intron-retained transcripts.

Main Results:

  • ASO targeting the slit3 splice site, but not the translation start site, disrupted pituitary axonal morphogenesis.
  • Observed increased expression of slit3, intron-retained transcripts, mir-218a-1, and slit2.
  • The observed phenotype was dependent on mir-218a-1 function and splicing of the upstream exon.
  • Intron-retained transcripts escaped nonsense-mediated decay (NMD), leading to increased functional microRNA expression.

Conclusions:

  • ASO-based targeting of intronic ncRNAs can lead to unintended increases in microRNA expression and function.
  • Intron-retained transcripts can evade NMD, contributing to altered ncRNA profiles.
  • The differential effects of splice- versus translation-blocking ASOs can serve as markers for identifying intronic microRNA functions.
  • Further validation is needed for other classes of ncRNAs and their therapeutic implications.