Research Spotlight: Insights into Toxoplasma gondii Differentiation
Citation: Lescault PJ, Thompson AB, Patil V, Lirussi D, Burton A, Margarit J, Bond J, Matrajt M. 2010. Genomic data reveal Toxoplasma gondii differentiation mutants are also impaired with respect to switching into a novel extracellular tachyzoite state. PLoS One. 2010 Dec 30;5(12):e14463.
Authors’ Association with MMG:
Pam Lescault – is an MMG Graduate Student
Ann Thompson – is an MMG Graduate Student
Veerupaxagouda Patil – is a former post-doc in Matrajt Lab
Dario Lirussi – is an MMG Graduate Student
Amanda Burton – is a former MMG Undergraduate Student
Juan Margarit – is a former technician in Matrajt Lab
Jeffrey Bond – is an MMG Associate Professor
Marianna Matrajt – is an MMG Assistant Professor
A critical portion of the lifecycle of the parasite Toxoplasma gondii is the invasion of host cells followed by replication of the tachyzoites and development of the parasite into the bradyzoite stage. Bradyzoites are a latent stage that can reside for long periods of time in host tissues and can be reactivated to generate fatal encephalitis in immune-compromised patients. Lescault and colleagues used microarray analysis of wild-type and mutant T. gondii to identify genes involved in the tachyzoite to bradyzoite transition. During this analysis they identified a novel extracellular tachyzoite stage that may be important for reinvasion of host cells during the acute phase of infection.
Impact and Significance:
T. gondii is an intracellular parasite of mammals whose primary host is the domestic cat. It is readily passed to humans who typically carry the parasite asymptomatically as intracellular bradyzoites. While bradyzoites rarely cause symptoms in healthy individuals, those with immune-deficiencies including people with AIDS and those undergoing chemotherapy are susceptible to potentially fatal toxoplasmosis. Understanding the gene regulation and proteins involved in the switch between bradyzoite and tachyzoite will be critical to identification of new therapeutic targets.