Journal
JOURNAL OF CELL SCIENCE
Volume 129, Issue 17, Pages 3320-3331Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.185223
Keywords
Cell division; Bradyzoite; Triclosan; Apicomplexa; Cleavage furrow
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Funding
- Indo-Brazil Collaborative Programme
- Department of Science and Technology, Ministry of Science and Technology (India) [DST/INT/BRAZIL RPO-01/2009/P-1]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [490440/2009-6]
- Coordencao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ)
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The apicomplexan protozoan Toxoplasma gondii, the causative agent of toxoplasmosis, harbors an apicoplast, a plastid-like organelle with essential metabolic functions. Although the FASII fatty acid biosynthesis pathway located in the apicoplast is essential for parasite survival, the cellular effects of FASII disruption in T. gondii had not been examined in detail. Here, we combined light and electron microscopy techniques-including focused ion beam scanning electron microscopy (FIB-SEM)-to characterize the effect of FASII disruption in T. gondii, by treatment with the FASII inhibitor triclosan or by inducible knockdown of the FASII component acyl carrier protein. Morphological analyses showed that FASII disruption prevented cytokinesis completion in T. gondii tachyzoites, leading to the formation of large masses of 'tethered' daughter cells. FIB-SEM showed that tethered daughters had a mature basal complex, but a defect in new membrane addition between daughters resulted in incomplete pellicle formation. Addition of exogenous fatty acids to medium suppressed the formation of tethered daughter cells and supports the notion that FASII is essential to generate lipid substrates required for the final step of parasite division.
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