Finally some time to cook!

Drafted the thesis 💃🎉, so hopefully 🤞 I’ll have time to clean the apartment and go to the gym 😅.

Любопытно открыть статью с огромным числом цитат и обнаружить там такое...

The phage and Erinnyis ello granulovirus NTase share catalytic motifs and show similar specificities for ligands used in cyclic nucleotide synthesis—namely, NTPs. 8.9/n

So, we first tried to elucidate the function for ORF55. We found it shares extreme similarity with the Chlorella virus DNA ligase, which is an ATP-dependent ligase with intrinsic nick sensing activity. 8.3/n

Phage ADPs that trigger bacterial defences have more homologs than other ADPs (p = 0.00129), and they often inhibit systems that degrade nucleic acids and induce abortive infection—suggesting bacteria adapt to prevalent phage threats with layered immunity. 7.2/n

We added ADPs to the network to visualise inhibitory interactions. Shared protein components suggest that an ADP targeting one defence could potentially inhibit others with similar structures—pointing to broader functional roles than previously recognised. 6.2/n

The study lacked direct interaction evidence, and we predicted a high-confidence model (ipTM = 0.87, pTM = 0.79, pDockQ = 0.634) showing that AcrIIA26 binds SpyCas9’s DNA-binding interface via its negatively charged surface. 5.8/n

The authors couldn’t tag AcrIB4 for direct incorporation studies, but we predicted a high-confidence interaction with Cas8b (ipTM = 0.91, pTM = 0.76, pDockQ = 0.424). 5.5/n

AcrIC3, from the same study, does not inhibit CRISPRi. Authors suggested it might block Cas3 recruitment or cleavage. We predicted a high-confidence interaction (ipTM = 0.91, pTM = 0.90, pDockQ = 0.633) between AcrIC3 and Cas3. 5.2/n

Example: AcrIC5 (doi: 10.1093/nar/gkab006) inhibits P. aeruginosa CRISPRi, likely by blocking DNA binding. Our model shows that AcrIC5 binds near the PAM site of PaCas8c (ipTM = 0.92, pTM = 0.85, pDockQ = 0.56). 5.1/n