Antiviral type III CRISPR signalling via conjugation of ATP and SAM
View abstract on PubMed
Summary
This summary is machine-generated.Type III-B CRISPR systems in Bacteroides fragilis use S-adenosyl methionine-AMP (SAM-AMP) for antiviral defense, not cyclic oligoadenylates. This novel second messenger targets membrane proteins, offering new insights into prokaryotic immunity.
Area Of Science
- Molecular Biology
- Microbiology
- Immunology
Background
- Prokaryotic CRISPR systems provide adaptive immunity against mobile genetic elements.
- Type III CRISPR systems utilize CRISPR RNA and Cas10 to detect and eliminate foreign nucleic acids.
- Some type III systems involve uncharacterized proteins like CorA and phosphodiesterases for defense.
Purpose Of The Study
- To investigate the antiviral defense mechanism of the CorA-associated type III-B (Cmr) CRISPR system from Bacteroides fragilis.
- To elucidate the signaling molecules and effectors involved in the B. fragilis Cmr system's immune response.
- To characterize the novel second messenger generated by this CRISPR system.
Main Methods
- Expression of the B. fragilis Cmr CRISPR system in Escherichia coli.
- Analysis of signaling molecules produced upon activation of the CRISPR system.
- Biochemical characterization of the interaction between the generated molecule and the CorA effector.
Main Results
- The B. fragilis Cmr system confers immunity against mobile genetic elements in E. coli.
- Instead of cyclic oligoadenylates, the system generates S-adenosyl methionine-AMP (SAM-AMP) by conjugating ATP to S-adenosyl methionine (SAM).
- SAM-AMP binds to the CorA effector, potentially disrupting membrane integrity and leading to cell dormancy or death.
Conclusions
- SAM-AMP is a novel class of second messenger involved in prokaryotic antiviral signaling.
- The B. fragilis Cmr system represents a distinct mechanism of type III CRISPR immunity.
- Degradation of SAM-AMP by specific enzymes provides a potential 'off switch' for the immune response.
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