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Codon-dependent transcriptional changes in response to tryptophan limitation in the tryptophan auxotrophic pathogens Chlamydia trachomatis and Streptococcus pyogenes

ABSTRACT: Codon-dependent transcriptional changes in response to tryptophan limitation in the tryptophan auxotrophic pathogens Chlamydia trachomatis and Streptococcus pyogenes

PROVIDER: PRJNA728014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14464900_1.fastq.gz	Fastqsanger.gz
	SRR14464900_2.fastq.gz	Fastqsanger.gz
	SRR14464901_1.fastq.gz	Fastqsanger.gz
	SRR14464901_2.fastq.gz	Fastqsanger.gz
	SRR14464833_1.fastq.gz	Fastqsanger.gz

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Codon-dependent transcriptional changes in response to tryptophan limitation in the tryptophan auxotrophic pathogens Chlamydia trachomatis and Streptococcus pyogenes

Project description:RNAseq analysis was performed for C. trachomatis serovar L2 and S. pyogenes NZ131 in the presence and absence of tryptophan to monitor transcriptional changes.

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Codon-Dependent Transcriptional Changes in Response to Tryptophan Limitation in the Tryptophan Auxotrophic Pathogens Chlamydia trachomatis and Streptococcus pyogenes.

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Project description:Chlamydia trachomatis (C. trachomatis) is an obligate intracellular bacterial pathogen responsible for trachoma and sexually transmitted infections. Like other Chlamydiota members, such as Waddlia chondrophila, C. trachomatis undergoes a biphasic developmental cycle alternating between infectious elementary bodies (EBs) and replicative reticulate bodies (RBs). Under stressful conditions, RBs differentiate into non-dividing aberrant bodies (ABs), a reversible state associated with persistence. Here, we investigate how early iron deprivation affects transcriptional regulation in C. trachomatis. We performed RNA sequencing to compare transcriptional profiles between EBs and RBs and between RBs and ABs induced by iron chelation with 2,2′-bipyridyl at 8 hpi. In EBs, 29% of genes were downregulated and 30% upregulated compared to RBs, revealing extensive transcriptional remodeling. At 24 hpi, ABs displayed downregulation of two-component system (TCS) genes (atoS, atoC, and chxR), while genes encoding inclusion membrane proteins (Incs) and the trpRBA operon were upregulated. These findings show how C. trachomatis adapts transcriptionally to iron deprivation, revealing stress- and time-dependent changes in metabolism, stress responses, and host–pathogen interactions. Persistence alters the developmental cycle while maintaining inclusion integrity and modulating host interactions, contributing to chronic infection. Uncovering the mechanisms driving persistence may offer crucial insights into chlamydial pathogenesis.

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Project description:Neutrophil granulocytes are the major cells involved in the Chlamydia trachomatis (C.trachomatis)-mediated inflammation and histopathology. A key gene in human intracellular antichlamydial defense is the tryptophan degrading enzyme indoleamine 2,3-dioxygenase (IDO), which limits the growth of the tryptophan auxotroph Chlamydia. Despite its importance, the role of IDO in the intracellular defense against Chlamydia in neutrophils has not yet been characterized. Affymetrix microarrays were used to obtain global gene expression data for monitoring the effect of C. trachomatis serovar D infection on the transcriptome of human neutrophil granulocytes.

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Project description:Limitation for amino acids is thought to regulate translation in mammalian cells primarily by signaling through the kinases mTORC1 and GCN2. We find that limitation for the amino acid arginine causes a selective loss of tRNA charging, which regulates translation through ribosome pausing at two of six arginine codons. Interestingly, limitation for leucine, an essential and abundant amino acid in protein, results in little or no ribosome pausing. Chemical and genetic perturbation of mTORC1 and GCN2 signaling revealed that their robust response to leucine limitation prevents ribosome pausing, while an insufficient response to arginine limitation led to loss of arginine tRNA charging and ribosome pausing. Codon-specific ribosome pausing decreased protein production and triggered premature ribosome termination without significantly reducing mRNA levels. Together, our results suggest that amino acids which are not optimally sensed by the mTORC1 and GCN2 pathways still regulate translation through an evolutionarily conserved mechanism based on synonymous codon usage.

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