Scot P. Ouellette

This study identifies Pkn1 kinase as a critical regulator of cell division in Chlamydia trachomatis by showing its localization at the division septum and its interaction with MreB.

This study shows that fluoroquinolone susceptibility in Chlamydia trachomatis depends on stage-specific DNA supercoiling levels, with treatment affecting growth and persistence through inhibition of DNA replication and gyrase activity.

This study characterizes AmiA_Ct, a peptidoglycan amidase in Chlamydia trachomatis, showing its role in degrading peptidoglycan during cell division and supporting normal growth and development.

This study shows that Chlamydia trachomatis TopA, containing a SWIB domain, mediates DNA relaxation and is essential for bacterial growth and host interaction.

This study shows that iron starvation of Chlamydia trachomatis increases host recognition of the pathogen by dysregulating a peptidoglycan enzyme, leading to inflammation and cell death.

This study shows that FtsK is essential for divisome assembly and septal peptidoglan synthesis in FtsZ-less Chlamydia trachomatis.

This study identifies c-di-AMP as a key factor triggering secondary differentiation in Chlamydia trachomatis by linking its levels to changes in EB production and gene transcription.

This study investigates how tryptophan starvation affects chlamydial inclusion membrane composition and host interactions during persistence.

This paper investigates the role of two anti-anti-sigma factors, RsbV1 and RsbV2, in the partner switching mechanism of Chlamydia trachomatis, showing that RsbV2 overexpression blocks secondary differentiation, reducing infectious EB production.

This study shows that altering the redox status of Chlamydia trachomatis affects its developmental cycle, with AhpC overexpression delaying differentiation and knockdown accelerating it.

The paper uses machine learning and metabolic modeling to show phosphoglycerate mutase is critical for Chlamydia trachomatis persistence under nutrient starvation.