Sean Czerwinski

@sczerwinski.bsky.social

529 Followers 980 Following

Ph.D. Candidate with @jamesgurney.bsky.social - Phage researcher that is open to losing or acquiring genes on occasion. he/him

Long contractile tailed bacteriophage in a yellow-gold environment.

Mutations in key regulatory factors of T4P biogenesis confer phage resistance. (A) PilR serves as the response regulator of pilA transcription. The sensor kinase, PilS, phosphorylates PilR, activating it, which, in turn, activates transcription of pilA, which encodes for the major pilin subunit, PilA. (B) PilZ regulates T4P biogenesis. By binding to the extension ATPase, PilB activates shaft polymerization. PilZ and FimX are necessary for PilB activation. (C) Without PilZ binding, PilB remains inactive, and energy is not generated for shaft assembly. (D) Defective PilR does not activate transcription of pilA, no PilA subunits are synthesized, and thus, the shaft is not assembled.

Chromosomal single-nucleotide polymorphisms (SNPs) defined for all co-evolution condition replicates and the ancestral PAO1. SNPs were determined using breseq (version 0.31). SNPs of two variations in 5 out of 5 (5/5) +Luz19 co-evo replicates and 3/5 +SA+Luz19 co-evo replicates. In all but one of these replicate sequences, the SNP in pilR is C192Y (TGC → TAC). Replicate B of the +Luz19 condition had a different SNP in pilR, P189Q (CCG → CAG). Of the replicates in the two conditions that were subject to co-evolution with Luz19, two lacked an SNP in pilR, both in the +SA+Luz19 condition. Replicate B instead had a 197 bp deletion in pilZ. Replicate A of +SA+Luz19 was the only replicate co-evolved alongside Luz19 that sequencing did not reveal a pil gene mutation; instead, a PQS system mutation was identified in pqsR.

Frozen marsh

Exoskeleton of a dead wheel bug