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Printable Handouts
Navigable Slide Index
- Introduction
- What A to I RNA editing is
- ADAR makes A to I changes in dsRNA
- Three mammalian ADAR genes
- Dramatic changes in functions of target genes
- A to I editing of mRNAs
- A global search for editing sites
- Global editing of repetitive sequences
- Human diseases of A to I RNA editing
- Diseases caused by ADAR1 deficiency
- ADAR1 is required for life
- Widespread apoptosis in ADAR1 null embryos
- Apoptosis and hepatitis in ADAR null mice livers
- DSH (Dyschromatosis Symmetrica Hereditaria)
- Human diseases caused by ADAR2 deficiency
- ADAR2 null mice die within weeks
- ALS and ischemia
- Diseases of 5HT2CR mRNA editing
- The 5HT2C receptor
- Editing sites within 5HT2CR mRNA
- Generation of 5HT2CR isoforms by editing
- Function of 5HT2CR mRNA editing
- Knock-in of VGV receptor
- Reduced growth of VGV mice
- Slim but not short VGV mice
- Control of appetite and energy balance
- Lower blood glucose / insulin levels in VGV mice
- Negative balance of energy in VGV mice
- Hyperphagic VGV mice
- Lean VGV mice
- Energetic VGV mice
- Beta-adrenergic receptor, UCP1 upregulation
- VGV affects SNS action, energy usage, lipolysis
- Metabolism, depression and schizophrenia
- A-to-I editing of microRNAs
- Editing of microRNAs in human diseases
- Controlling miRNA target selection
- MiR-376 cluster RNAs are highly edited at 2 sites
- Site editing by ADAR1 and ADAR2
- Editing frequency varied in different tissues
- Both ADAR sites located within seed sequence
- Identifying candidate target genes
- Target genes predicted for unedited miR-376a-5p
- Target genes predicted for edited miR-376a-5p
- Differential repression
- In vivo significance of miR 376a editing
- Phosphoribosyl pyrophosphate synthetase 1 (1)
- Phosphoribosyl pyrophosphate synthetase 1 (2)
- Uric acid levels in ADAR null tissues v. WT
- Importance of uric acid
- Biological significance of miR-376a RNA editing
- Control of miRNA expression/functions by editing
- Summary
Topics Covered
- What is A-to-I RNA editing?
- Human diseases caused by ADAR1 deficiency
- Human diseases caused by ADAR2 deficiency
- Human diseases of 5-HT2CR mRNA editing
- Human pathological conditions caused by deficiency in microRNA editing
Talk Citation
Nishikura, K. (2013, January 17). A-to-I RNA editing in human disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved September 1, 2024, from https://doi.org/10.69645/TMOJ6950.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Kazuko Nishikura has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Cell Biology
Transcript
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0:00
Hello, I'm Kazuko Nishikura,
a professor at the Wistar Institute
in Philadelphia.
0:09
Today, I'm going to
talk about RNA editing.
RNA editing is
a post-transcriptional process that
changes the nucleotide
sequence of an RNA transcript,
resulting in different RNA not
encoded in the genomic DNA.
There are many different types of RNA
editing that modify transcripts of plant,
animal and parasite genomes as
described in Dr Stephen Hajduk's talk.
One particular type of RNA editing
changes adenosine to inosine.
I will talk about this A-to-I RNA editing,
and
especially about its
relevance to human diseases.
ADAR (adenosine deaminase acting
on RNA) is an enzyme involved
0:56
in this A-to-I RNA editing process and
converts adenosine to inosine,
specifically in double-stranded RNAs
through a hydrolytic deamination reaction.
Inosine base-pairs with cytidine and
is treated as
if it were guanosine by
the translation machinery.
Reverse transcriptase also
reads inosine as guanosine,
so A-to-I RNA editing can be detected as
an A-to-G change in the cDNA sequence.
1:39
We identified the first member
of the ADAR gene family ADAR1,
which subsequently led
to identification of two
additional family members,
ADAR2 and ADARs3.
These ADARs are highly
conserved from fish to human.
ADARs share a common
substrate-binding domain containing
two to three repeats of
a double-strand RNA binding motif and
a common deaminase or catalytic domain.
Additional domains
are unique to each member,
such as the Z DNA binding
domain of ADAR1 and
the arginine-lysine-rich single-strand
RNA binding R-domain of ADAR3.
Both ADAR1 and
ADAR2 are detected in many tissues,
whereas ADAR3 is expressed
only in the brain.