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lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA (lncRNA)...

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Related Experiment Video

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Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry

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Published on: May 17, 2016

A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA.

Marcella Cesana¹, Davide Cacchiarelli, Ivano Legnini

¹Department of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, Italy.

|October 18, 2011

Summary

A novel muscle-specific long noncoding RNA, linc-MD1, acts as a competing endogenous RNA (ceRNA) to control muscle differentiation timing. Its dysregulation impacts muscle development and is reduced in Duchenne muscular dystrophy.

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Area of Science:

Molecular Biology
Genetics
Developmental Biology

Background:

RNA crosstalk via competing endogenous RNAs (ceRNAs) offers a layer of post-transcriptional regulation.
ceRNAs modulate microRNA (miRNA) distribution, influencing gene expression.

Purpose of the Study:

Identify novel ceRNAs involved in muscle differentiation.
Investigate the role of linc-MD1 in regulating myogenesis.
Determine the therapeutic potential of targeting ceRNAs in muscle disorders.

Main Methods:

RNA sequencing and expression analysis in mouse and human myoblasts.
Functional assays involving linc-MD1 knockdown and overexpression.
Validation of miRNA-target interactions using luciferase assays and Western blotting.

Main Results:

linc-MD1 acts as a muscle-specific ceRNA, sponging miR-133.
linc-MD1 regulates MAML1 and MEF2C expression, key transcription factors for muscle differentiation.
linc-MD1 controls differentiation timing in both mouse and human myoblasts.
Reduced linc-MD1 levels observed in Duchenne muscular dystrophy patient cells.

Conclusions:

The ceRNA network, particularly linc-MD1, is crucial for regulating muscle differentiation timing.
linc-MD1 represents a potential therapeutic target for muscle-related diseases.
Dysregulation of linc-MD1 contributes to the pathology of Duchenne muscular dystrophy.