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RNA Interference

RNA Interference

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.
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...

RNA Interference

RNA Interference

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.
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...

siRNA - Small Interfering RNAs

siRNA - Small Interfering RNAs

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.
In the cytoplasm, siRNA is processed from a double-stranded RNA, which comes from either endogenous DNA transcription or exogenous sources like a virus. This double-stranded RNA is then cleaved by the ATP-dependent...

Experimental RNAi

Experimental RNAi

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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Related Experiment Video

Updated: Jun 12, 2026

Shifting Zebrafish Lethal Skeletal Mutant Penetrance by Progeny Testing

Shifting Zebrafish Lethal Skeletal Mutant Penetrance by Progeny Testing

Published on: September 1, 2017

Second generation lethality in RNAseH2a knockout zebrafish.

Ruth C Thomas^1,2, Ringaile Zaksauskaite^1,2, Norah Y Al-Kandari^1,2

¹Bateson Centre, School of Biosciences, University of Sheffield, Sheffield S10 2TN, UK.

Nucleic Acids Research

|September 1, 2024

Summary

This summary is machine-generated.

Zebrafish lacking RNaseH2a show minimal adult defects but their offspring experience embryonic lethality due to DNA fragmentation. This highlights a novel mechanism of genome instability and developmental failure.

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Area of Science:

Genetics
Molecular Biology
Developmental Biology

Background:

Ribonucleotide removal from DNA by RNaseH2 is crucial for genome stability.
Impaired RNaseH2 function is linked to the neurodegenerative disorder Aicardi Goutières Syndrome.

Purpose of the Study:

To create and analyze a zebrafish rnaseh2a mutant model for studying RNaseH2 function.
To investigate the long-term effects of RNaseH2a deficiency on genome stability and development.

Main Methods:

Generation of a zebrafish rnaseh2a mutant line.
Phenotypic analysis of first and second-generation offspring.
Assessment of ribonucleotide incorporation and inflammatory markers.
Examination of DNA integrity and embryonic lethality.

Main Results:

First-generation RNaseH2a knockout zebrafish adults exhibit few abnormalities.
Second-generation offspring display developmental delays, increased ribonucleotide incorporation, and inflammation.
Maternal and paternal embryonic lethality observed in second-generation crosses.
Accumulation of ribonucleotides in adult brain and testes of rnaseh2a-/- zebrafish.
Identification of ribodysgenesis (rNMP removal and DNA fragmentation) as the cause of lethality.

Conclusions:

Zebrafish possess RNaseH2-independent compensatory mechanisms that are insufficient in offspring.
Inherited ribonucleotides overwhelm compensatory pathways, leading to embryonic lethality.
Ribodysgenesis is a novel mechanism contributing to genome instability and developmental failure in this model.