The Transforming Parasite Theileria Co-opts Host Cell Mitotic and Central Spindles to Persist in Continuously Dividing Cells

Schubert, Conrad von; Xue, Gui-Rong; Schmuckli‐Maurer, Jacqueline; Woods, Kerry; Nigg, Erich A.; Dobbelaere, D. A. E.

doi:10.1371/journal.pbio.1000499

Cited by 70 publications

(93 citation statements)

References 74 publications

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“…Rab6 and 11 are both recruited to the C. trachomatis inclusion membrane (42); moreover, Rab6-or Rab11-positive vesicles localize to the equatorial cell cortex during anaphase (21,52), implicating a possible role for these GTPases in trafficking the inclusion during cell division. A recent study on Theileria showed that the parasite can recruit host Plk1 and localize to the host central spindle (50). Unlike Theileria, none of the host signaling proteins that we examined were noticeably recruited to the Chlamydia inclusion membrane.…”

Section: Discussioncontrasting

confidence: 57%

Chlamydia trachomatis Inclusions Induce Asymmetric Cleavage Furrow Formation and Ingression Failure in Host Cells

Sun

Wilde

Harrison

2011

Molecular and Cellular Biology

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Chlamydia trachomatis infection has been suggested to induce host genome duplication and is linked to increased risks of cervical cancer. We describe here the mechanism by which Chlamydia causes a cleavage furrow defect that consistently results in the formation of multinucleated host cells, a phenomenon linked to tumorigenesis. Host signaling proteins essential for cleavage furrow initiation, ingression, and stabilization are displaced from one of the prospective furrowing cortices after Chlamydia infection. This protein displacement leads to the formation of a unique asymmetrical, unilateral cleavage furrow in infected human cells. The asymmetrical distribution of signaling proteins is caused by the physical presence of the Chlamydia inclusion at the cell equator. By using ingested latex beads, we demonstrate that the presence of a large vacuole at the cell equator is sufficient to cause furrow ingression failure and can lead to multinucleation. Interestingly, internalized latex beads of similar size do not localize to the cell equator as efficiently as Chlamydia inclusions; moreover, inhibition of bacterial protein synthesis with antibiotic reduces the frequency at which Chlamydia localizes to the cell equator. Together, these results suggest that Chlamydia effectors are involved in strategic positioning of the inclusion during cell division.

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Section: Discussioncontrasting

confidence: 57%

Chlamydia trachomatis Inclusions Induce Asymmetric Cleavage Furrow Formation and Ingression Failure in Host Cells

Sun

Wilde

Harrison

2011

Molecular and Cellular Biology

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“…Theileria annulata indicates that T. lestoquardi schizont can lead to metastasis and uncontrolled proliferation of the infected leukocyte to the non-lymphoid tissues, which is very similar to the multiplication in the lymphoid tissues (Dobbelaere and Küenzi, 2004;Von Schubert et al, 2010). According to a previous study, macroschizont and microschizont have been found in the liver, spleen, lung, kidney, and lymph nodes in sheep (Yin et al, 2003).…”

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confidence: 86%

An experimental ovine Theileriosis: The effect of Theileria lestoquardi infection on cardiovascular system in sheep

et al. 2016

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“…Perhaps the most striking example of dependence on host cell cycle progression in protozoan parasites comes from the apicomplexans Theileria annulata and Theileria parva, which ensure their own propagation by transforming the lymphocytes and monocytes they infect (reviewed in reference 10). During continuous rounds of cell cycle progression and mitosis, they align themselves to the host mitotic spindle for distribution into both daughter cells during cytokinesis (11).…”

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confidence: 99%

In Vitro Alterations Do Not Reflect a Requirement for Host Cell Cycle Progression during Plasmodium Liver Stage Infection

Hanson

March

et al. 2015

Eukaryot Cell

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f Prior to invading nonreplicative erythrocytes, Plasmodium parasites undergo their first obligate step in the mammalian host inside hepatocytes, where each sporozoite replicates to generate thousands of merozoites. While normally quiescent, hepatocytes retain proliferative capacity and can readily reenter the cell cycle in response to diverse stimuli. Many intracellular pathogens, including protozoan parasites, manipulate the cell cycle progression of their host cells for their own benefit, but it is not known whether the hepatocyte cell cycle plays a role during Plasmodium liver stage infection. Here, we show that Plasmodium parasites can be observed in mitotic hepatoma cells throughout liver stage development, where they initially reduce the likelihood of mitosis and ultimately lead to significant acquisition of a binucleate phenotype. However, hepatoma cells pharmacologically arrested in S phase still support robust and complete Plasmodium liver stage development, which thus does not require cell cycle progression in the infected cell in vitro. Furthermore, murine hepatocytes remain quiescent throughout in vivo infection with either Plasmodium berghei or Plasmodium yoelii, as do Plasmodium falciparum-infected primary human hepatocytes, demonstrating that the rapid and prodigious growth of liver stage parasites is accomplished independent of host hepatocyte cell cycle progression during natural infection.

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The Transforming Parasite Theileria Co-opts Host Cell Mitotic and Central Spindles to Persist in Continuously Dividing Cells

Abstract: The transforming protozoan Theileria recruits Plk1, a host kinase that regulates mitosis, to its surface and engages spindle microtubules to secure its division and inheritance into both daughter cells.

Cited by 70 publications

References 74 publications

Chlamydia trachomatis Inclusions Induce Asymmetric Cleavage Furrow Formation and Ingression Failure in Host Cells

Chlamydia trachomatis Inclusions Induce Asymmetric Cleavage Furrow Formation and Ingression Failure in Host Cells

An experimental ovine Theileriosis: The effect of Theileria lestoquardi infection on cardiovascular system in sheep

In Vitro Alterations Do Not Reflect a Requirement for Host Cell Cycle Progression during Plasmodium Liver Stage Infection

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