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Page 12 of 17 Wottrich et al. Microbiome Res Rep 2024;3:27 https://dx.doi.org/10.20517/mrr.2023.42

Figure 5. Protein signatures of Phage TP-J34 Ltp and Phage Aquarius gp41. (A) Phage TP-J34 Ltp. Output from InterPro (blue) indicated
the presence of several protein signatures, including the two conserved domains that comprise the active site region of Ltp (residues 49-
92 and 96-141). Other notable signatures included a prokaryotic lipoprotein (residues 1-20), regions of disorder (residues 21-50 and 21-
37), signal peptide H-region (residues 4-15), signal peptide C-region (residues 16-20), signal peptide N-region (residues 1-3), signal
peptide (residues 1-20), transmembrane signal peptide (residues 1-28), and a non-cytoplasmic domain (residues 21-142). Output from
MEME (red) indicated the presence of two conserved motifs as well, spanning residues 46-77 and 91-141. Output from RaptorX (green;
depicted on ruler) also identified a generally high region of disorder spanning from the first residue to roughly residue 50, and a small
region at the very end of the peptide spanning roughly one to two residues; (B) Protein signatures of Phage Aquarius gp41. Output from
InterPro (blue) indicated the presence of several notable protein signatures, including regions of disorder (residues 23-89 and 34-51),
signal peptide H-region (residues 8-19), signal peptide C-region (residues 20-24), signal peptide N-region (residues 1-7), signal peptide
(residues 1-24), transmembrane signal peptide (residues 1-25), transmembrane helix (residues 7-26), and a non-cytoplasmic domain
(residues 25-179). Output from MEME (red) indicated the presence of two conserved motifs as well, spanning residues 84-133 and 137-
177. Output from RaptorX (green; depicted on ruler) also identified a generally high region of disorder spanning from the first residue to
roughly residue 91, and a small region at the very end of the peptide spanning roughly three to five residues. MEME: Multiple Em for
Motif Elicitation.

still able to initiate the lytic life cycle but produce fewer progeny phages per time (lower multiplicity of
infection). Thus, rather than being completely inhibited from superinfecting, these secondary infecting
phages have lower fitness than the initial phage that was infected [56,57] . Other phages, such as T4 which