<i>Chlamydia</i> preserves the mitochondrial network necessary for replication via microRNA-dependent inhibition of fission

Chowdhury, Suvagata Roy; Reimer, Anastasija; Sharan, Malvika; Kozjak-Pavlovic, Vera; Eulálio, Ana; Prusty, Bhupesh K.; Fraunholz, Martin; Karunakaran, Karthika; Rudel, Thomas

doi:10.1083/jcb.201608063

Cited by 98 publications

(91 citation statements)

References 88 publications

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“…By contrast, Chlamydia trachomatis preserves the elongated mitochondrial network for its intracellular proliferation. C. trachomatis upregulates a host miRNA (miR-30c-5p), which is key in maintaining the mitochondrial structure and intracellular proliferation of the bacteria [21]. While during the early infection phase, C. trachomatis induces mitochondrial elongation, it does resort to enhancing mitochondrial fragmentation during the late phases of infection [22].…”

Section: Modulation Of Mitochondrial Dynamics Upon Infectionmentioning

confidence: 99%

Mitochondrial Functions in Infection and Immunity

Tiku¹,

Tan²,

Đikić

2020

Trends in Cell Biology

266

208

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Section: Modulation Of Mitochondrial Dynamics Upon Infectionmentioning

confidence: 99%

Mitochondrial Functions in Infection and Immunity

Tiku¹,

Tan²,

Đikić

2020

Trends in Cell Biology

266

208

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“…We have recently shown by high‐throughput sequencing that Chlamydia infection affects the miRNAome of host cells (Chowdhury et al, ). Wild‐type Chlamydia infection upregulated miR‐499a (Figure a), which regulates the expression of polymerase β by binding to a seed region within the 3'UTR (Wang et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…Our data show that in cells infected with Chlamydia, BER can be improved by interfering with miR-499a expression and thereby stabilising polymerase β. Chlamydia. Because stabilisation of p53 interferes with chlamydial development, p53 is downregulated during infection by several mechanisms such as activating PI3K pathway, stabilising MDM2, and upregulating miR-30c (Chowdhury et al, 2017;González et al, 2014;Siegl et al, 2014). Moreover, it has been shown in both in vitro and in vivo studies that p53 directly plays a role in BER not only by stabilising the repair complexes on the DNA but also by directly modulating polymerase-β expression in mouse fibroblasts (Seo et al, 2002;Zhou et al, 2001).…”

Section: We Have Recently Shown By High-throughput Sequencing Thatmentioning

confidence: 99%

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Chlamydia trachomatis impairs host base excision repair by downregulating polymerase β

Gulve

Prusty

Rudel

2019

Cellular Microbiology

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Chlamydia trachomatis infections have been associated with ovarian cancer by several epidemiological studies. Here, we show that C. trachomatis‐infected primary human ovarian epithelial cells display elevated oxidative DNA damage. Base excision repair, an important cellular mechanism to repair oxidative DNA lesions, was impaired in infected primary ovarian and in several other types of cells. Polymerase β was downregulated in infected cells associated with upregulation of microRNA‐499a (miR‐499a). Stabilising polymerase β by inhibiting miR‐499a significantly improved repair. Moreover, downregulation of tumour suppressor p53 also resulted in attenuated repair in these cells. Thus, our data show that downregulation of polymerase β by direct inhibition through miR‐499a and downregulation of p53 debilitate the host‐cell base excision repair during C. trachomatis infection.

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“…Structural alterations to mitochondria during C . trachomatis infection have been described (Chowdhury et al, ). Such alterations may be linked to reduced synthesis of these protein groups.…”

Section: Discussionmentioning

confidence: 99%

Infection of HeLa cells with Chlamydia trachomatis inhibits protein synthesis and causes multiple changes to host cell pathways

Ohmer

Tzivelekidis

Niedenführ

et al. 2019

Cellular Microbiology

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The obligate intracellular bacterium Chlamydia trachomatis replicates in a cytosolic vacuole in human epithelial cells. Infection of human cells with C. trachomatis causes substantial changes to many host cell‐signalling pathways, but the molecular basis of such influence is not well understood. Studies of gene transcription of the infected cell have shown altered transcription of many host cell genes, indicating a transcriptional response of the host cell to the infection. We here describe that infection of HeLa cells with C. trachomatis as well as infection of murine cells with Chlamydia muridarum substantially inhibits protein synthesis of the infected host cell. This inhibition was accompanied by changes to the ribosomal profile of the infected cell indicative of a block of translation initiation, most likely as part of a stress response. The Chlamydia protease‐like activity factor (CPAF) also reduced protein synthesis in uninfected cells, although CPAF‐deficient C. trachomatis showed no defect in this respect. Analysis of polysomal mRNA as a proxy of actively transcribed mRNA identified a number of biological processes differentially affected by chlamydial infection. Mapping of differentially regulated genes onto a protein interaction network identified nodes of up‐ and down‐regulated networks during chlamydial infection. Proteomic analysis of protein synthesis further suggested translational regulation of host cell functions by chlamydial infection. These results demonstrate reprogramming of the host cell during chlamydial infection through the alteration of protein synthesis.

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Chlamydia preserves the mitochondrial network necessary for replication via microRNA-dependent inhibition of fission

Abstract: Chlamydiae are intracellular pathogens that depend on the host for their survival and development. Chowdhury et al. demonstrate that Chlamydia trachomatis infection can prevent mitochondrial fission in primary cells by reducing DRP1 abundance via miR-30c–dependent inhibition of p53.

Cited by 98 publications

References 88 publications

Mitochondrial Functions in Infection and Immunity

Mitochondrial Functions in Infection and Immunity

Chlamydia trachomatis impairs host base excision repair by downregulating polymerase β

Infection of HeLa cells with Chlamydia trachomatis inhibits protein synthesis and causes multiple changes to host cell pathways

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