Department of Global Health, University of South Florida, Tampa, FL, 33612, USA.
Cell Microbiol. 2014 Apr;16(4):466-72. doi: 10.1111/cmi.12267. Epub 2014 Feb 16.
Toxoplasma gondii exhibits a complex, multi-stage life cycle in which the need for parasite expansion is balanced with the production of transmissible forms. For human disease the key developmental switch is from the tachyzoite to the mature bradyzoite, which is not well understood at the molecular level. This review highlights the role of the tachyzoite in regulating the initiation of bradyzoite differentiation through newly discovered transcription factors of the ApiAP2 family that must be turned off for development to unfold. Exit from the tachyzoite cell cycle is also tightly co-ordinated with the induction of bradyzoite gene expression, which is strongly influenced by the host cell environment. New evidence suggests a parasite casein kinase II and host anti-growth factor CDA1 can influence specific pathways that are responsible for sensing the host cell environment and informing the parasites decision to continue replication or to develop into bradyzoites. These results indicate tachyzoite gene expression mechanisms and signal transduction pathways likely hold the keys to tissue cyst formation in Toxoplasma.
刚地弓形虫表现出复杂的多阶段生命周期，在该周期中，寄生虫的扩张需求与可传播形式的产生相平衡。对于人类疾病，关键的发育开关是从速殖子到成熟的缓殖子，而这在分子水平上还不是很清楚。这篇综述强调了速殖子在调节缓殖子分化启动中的作用，通过新发现的 ApiAP2 家族转录因子来调节，这些转录因子必须关闭才能进行发育。退出速殖子细胞周期也与缓殖子基因表达的诱导紧密协调，这受到宿主细胞环境的强烈影响。新的证据表明，寄生虫酪蛋白激酶 II 和宿主抗生长因子 CDA1 可以影响负责感知宿主细胞环境并告知寄生虫继续复制或发育成缓殖子的特定途径。这些结果表明，速殖子基因表达机制和信号转导途径可能是刚地弓形虫组织包囊形成的关键。
