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Experimental RNAi

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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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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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Related Experiment Video

Updated: Jul 6, 2026

RNAi Mediated Gene Knockdown and Transgenesis by Microinjection in the Necromenic Nematode Pristionchus pacificus

RNAi Mediated Gene Knockdown and Transgenesis by Microinjection in the Necromenic Nematode Pristionchus pacificus

Published on: October 16, 2011

Prnp knockdown in transgenic mice using RNA interference.

Micaela Gallozzi¹, Jérome Chapuis, Fabienne Le Provost

¹UR 339, Laboratoire de Génétique Biochimique et de Cytogénétique, Institut National de la Recherche Agronomique, 78350, Jouy-en-Josas, France.

Transgenic Research

|March 20, 2008

Summary

RNA interference effectively reduced prion protein gene expression in mice. This gene knockdown approach shows promise for disease resistance, though expression levels impact efficiency.

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Last Updated: Jul 6, 2026

RNAi Mediated Gene Knockdown and Transgenesis by Microinjection in the Necromenic Nematode Pristionchus pacificus

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Published on: October 16, 2011

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Published on: April 10, 2018

Area of Science:

Molecular Biology
Genetics
Neuroscience

Background:

RNA interference (RNAi) is a powerful tool for gene knockdown in various organisms.
The prion protein (PrP) is implicated in neurodegenerative diseases.

Purpose of the Study:

To develop and test an RNA interference strategy targeting the prion protein mRNA.
To assess the efficacy of this approach in reducing endogenous Prnp gene expression in transgenic mice.

Main Methods:

Designed a microRNA (miRNA) targeting prion protein mRNA.
Expressed the miRNA using the human PRNP promoter in cell cultures and transgenic mice.
Quantified Prnp gene expression levels in transfected cells and mouse lines.

Main Results:

Confirmed miRNA efficiency in transfected cells.
Generated several transgenic mouse lines expressing the designed miRNA.
Observed significant downregulation of endogenous mouse Prnp gene expression, up to 80% inhibition.
Found a correlation between transgene expression level and Prnp gene downregulation.

Conclusions:

RNA interference is a viable strategy for targeting Prnp gene expression.
The efficiency of RNAi-mediated gene knockdown is dependent on transgene expression levels.
This approach holds potential for developing disease resistance strategies against prion diseases, with noted limitations.