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Rickettsia parkeri strain:Black Gap

ABSTRACT: Rickettsia parkeri strain:Black Gap Genome sequencing

PROVIDER: PRJNA699590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR14704664.fastq.gz	Fastqsanger.gz
	SRR15947633_1.fastq.gz	Fastqsanger.gz
	SRR15947633_2.fastq.gz	Fastqsanger.gz
	SRR15947634_1.fastq.gz	Fastqsanger.gz

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The ankyrin repeat protein RARP-1 is a periplasmic factor that supports Rickettsia parkeri growth and host cell invasion

Project description:Rickettsia spp. are obligate intracellular bacterial pathogens that have evolved a variety of strategies to exploit their host cell niche. However, the bacterial factors that contribute to this intracellular lifestyle are poorly understood. Here, we show that the conserved ankyrin repeat protein RARP-1 supports Rickettsia parkeri infection. Specifically, RARP-1 promotes efficient host cell entry and growth within the host cytoplasm, but is not necessary for cell-to-cell spread or evasion of host autophagy. We further demonstrate that RARP-1 is not secreted into the host cytoplasm by R. parkeri. Instead, RARP-1 resides in the periplasm, and we identify several binding partners that are predicted to work in concert with RARP-1 during infection. Altogether, our data reveal that RARP-1 plays a critical role in the rickettsial life cycle.

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RNA-seq reveals genes regulated by type I interferon during Rickettsia infection in WT and Irf-deficient bone marrow-derived macrophages

Project description:We report transcript abundance in murine bone marrow-derived macrophages (BMDMs) upon Rickettsia parkeri infection and treatment with type I interferon (IFN-I). Infections and IFN-I treatment were performed in parallel between WT BMDMs and BMDMs lacking genes encoding interferon-responsive factor (IRF) transcription factors, including IRF1, IRF5, and double mutant cells lacking both IRF3 and IRF7. Control cells were uninfected and not treated with IFN-I. The abundance of transcripts between these cells can be compared in order to identify genes specifically regulated by each IRF upon IFN-I treatment.

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