Toxoplasma gondii exploits UHRF1 and induces host cell cycle arrest at G2 to enable its proliferation

被引：74

作者：

Brunet, Julie ^{[1
]}

Pfaff, Alexander W. ^{[1
]}

Abidi, Ahmed ^{[1
]}

Unoki, Motoko ^{[2
]}

Nakamura, Yusuke ^{[3
]}

Guinard, Marie ^{[1
]}

Klein, Jean-Paul ^{[1
]}

Candolfi, Ermanno ^{[1
]}

Mousli, Marc ^{[1
]}

机构：

[1] Univ Strasbourg, Fac Med, Inst Parasitol & Pathol Tropicale Strasbourg, UPRES EA Interact Cellulaires & Mol Hote Paraite, F-67000 Strasbourg, France

[2] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA

[3] Univ Tokyo, Inst Med Sci, Mol Med Lab, Ctr Human Genome, Tokyo, Japan

来源：

CELLULAR MICROBIOLOGY | 2008年 / 10卷 / 04期

关键词：

D O I：

10.1111/j.1462-5822.2007.01093.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

Toxoplasma gondii is an obligate intracellular parasite that causes severe disease in humans. It is able to infect all nucleated mammalian cells leading to lifelong persistence of the parasite in the host. Here, we studied the effect of T. gondii infection on host cell proliferation and explored the molecular mechanisms involved in host cell cycle progression. We found that T. gondii induced G1/S transition in host cells in the presence of UHRF1, followed by G2 arrest after cyclin B1 downregulation which is probably the major cause of the arrest. Other molecules at the G2/M checkpoint including p53, p21 and Cdk1 were normally regulated. Interestingly, while parasite proliferation was normal in cells that were in the G2 phase, it was suppressed in G1-arrested cells induced by UHRF1-siRNA, indicating the importance of the G2 phase via UHRF1-induced G1/S transition for T. gondii growth.

引用

页码：908 / 920

页数：13

共 48 条

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