Thursday, April 12, 2012

Cactin is essential for G1 progression in Toxoplasma gondii

Mol Microbiol. 2012 Apr 9. doi: 10.1111/j.1365-2958.2012.08044.x. [Epub ahead of print]

Cactin is essential for G1 progression in Toxoplasma gondii.

Szatanek T, Anderson-White BR, Faugno-Fusci DM, White M, Saeij JP, Gubbels MJ.

SourceDepartment of Biology, Boston College, Chestnut Hill, MA 02467, USA Departments of Molecular Medicine & Global Health, Florida Center for Drug Discovery and Innovation, Colleges of Medicine & Public Health, University of South Florida, Tampa, FL 33612, USA Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Abstract
Toxoplasma gondii is an obligate intracellular protozoan parasite whose rapid lytic replication cycles define its pathogenicity. We identified a temperature-sensitive growth mutant, FV-P6, which irreversibly arrests before the middle of the G1 stage of the tachyzoite cell cycle. This arrest is caused by a point mutation in a gene conserved across eukaryotes, Cactin, whose product localizes to the nucleus. To elucidate the role of TgCactin we performed genome-wide expression profiling. Besides the expected G1 expression profile, many genes associated with the extracellular state as well as with the bradyzoite cyst stage were identified. Consistent with these profiles were the expression of AP2 transcription factors typically associated with extracellular and bradyzoite stage parasites. This suggests a role for TgCactin in control of gene expression. As TgCactin does not contain any functionally defined domains we reasoned TgCactin exerts its function through interactions with other proteins. In support of this model we demonstrated that TgCactin is present in a protein complex and can oligomerize. Taken together, these results suggest that TgCactin acts as a pivotal protein potentially regulating gene expression at several transition points in parasite development.

© 2012 Blackwell Publishing Ltd.

PMID: 22486860 [PubMed - as supplied by publisher]

No comments: