1. Type III CRISPR-Cas systems in prokaryotes provide immunity against invading nucleic acids through the coordinated degradation of transcriptionally active DNA and its transcripts by the Csm effector complex.
2. Target RNA binding by the Csm effector complex triggers Cas10 to synthesize cyclic oligoadenylates (cA n ; n = 2 to 6) by means of the Palm domains, which act as signaling molecules to bind Csm6 and activate its nonspecific RNA degradation.
3. This cyclic oligoadenylate-based signaling pathway coordinates different components of CRISPR-Cas to prevent phage infection and propagation.
The article is written in a clear and concise manner, providing a comprehensive overview of the research conducted on type III CRISPR-Cas systems in prokaryotes. The authors present their findings in an unbiased way, providing evidence for their claims and exploring potential counterarguments. The article does not contain any promotional content or partiality, and all possible risks are noted throughout the text. Furthermore, both sides of the argument are presented equally, with no one-sided reporting or unsupported claims. The only potential issue with this article is that it does not explore other potential pathways for phage infection prevention beyond the cyclic oligoadenylate-based signaling pathway discussed in detail. However, this is likely due to the scope of the research conducted rather than any bias on behalf of the authors. In conclusion, this article can be considered reliable and trustworthy overall.