Link to this post | posted 08 Nov, 2025 03:38
debbie	Ping, I would not do that. The lysogen could technically (though unlikely) be to the other phage. It would be helpful to have a pcr designed to show integration….. I would recommend testing other DC1 phages on the lysogen. debbie

Link to this post | posted 07 Nov, 2025 22:21
debbie	Ping, My best suggestion is to plate for single plaques, and pick a plaque that represents the majority of phenotypes THAT IS WELL ISOLATED FROM OTHERS PLAQUES and make a new stock. You can PCR to confirm, but not rule out contamination. When purifying, pick early. I hope that makes sense. best, debbie

Link to this post | posted 07 Nov, 2025 18:47

debbie

Hi Ping, You have a seqeunce right? And you have identified the repressor. You can compare it to other DC1 phage sequences. And you have other DC1 phages in your U of Pittsburgh collection. Test those! Consider compiling the data of DC1 phages, their infections patterns and their genomic comparisons (especially of the repressor sequence). And note that the simplest answer may be the best one - is your lysate pure? And I agree with Vic - grids of dilutions presented in a comparative way (when you repeat) will produce publication quality pictures. debbie

Link to this post | posted 07 Nov, 2025 15:50

debbie

If both phages have the same repressor, then a lysogen of one should not be infected by the other phage. We have examples where the phages of the same cluster do infect a lysogen, but their repressor is broken/absent. We also have examples where a phage can carry 2 different repressors (why not, right?) and keep keep out phages of a different cluster. in order for a phage to maintain lysogeny, a repressor can be essential. Papers include Cell, 2023. Other papers of D29. A paper about phage Tweety…. Lots of examples. debbie

Link to this post | posted 31 Oct, 2025 13:09
debbie	Thanks Rick! Christine - I would follow Rick's advice! debbie

Link to this post | posted 30 Oct, 2025 01:56
debbie	Hi Haley and Christine, I don't believe that there is enough evidence to calla function for this protein. Be sue to document this call when submitting it. Include this post in your cover sheet. Thanks, debbie

Link to this post | posted 22 Oct, 2025 15:00
debbie	Nope! But provide that here and I will add that to the function list, so others can pick the best model number. Would that work? Also provide me with the list of genes that you have called. I can add them as examples too. Thanks, debbie

Link to this post | posted 22 Oct, 2025 14:51
debbie	Hi Peter, We are going to cautiously weigh in on what to name the various structures of siphoviruses. The data is coming to us fast and furious, and not all crystallographers are using the same nomenclature. I have added the features (as you have identified)to the Approved Function List that I think we can call with a modicum of confidence. Let me know if my list works! Thanks, debbie

Link to this post | posted 21 Oct, 2025 19:31
debbie	Hi Brian, The difference in the gene count is that PECAAN is not counting tRNAs. I don't believe that there is a gene duplication per se. regardless, that is why the curation work that you and your students do is so important! Happy annotating! Best, debbie

Link to this post | posted 02 Oct, 2025 01:05
debbie	HI Brian, When I look at the Starterator report, I see one common start for every phage listed - it is technically threaded through the starts listed as 9, 10 and 11. Which is the start that corresponds to bp 110. Remember that starterator is a clustal alignment and as the sequence diverges, small discrepancies at the nucleotide level can be present. I would call 110 as the start. debbie