Leitsch David, Köhsler Martina, Marchetti-Deschmann Martina, Deutsch Andrea, Allmaier Günter, Duchêne Michael, Walochnik Julia
Department of Specific Prophylaxis and Tropical Medicine, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Eukaryot Cell. 2010 Apr;9(4):611-8. doi: 10.1128/EC.00300-09. Epub 2010 Feb 26.
Acanthamoeba castellanii is a facultative pathogen that has a two-stage life cycle comprising the vegetatively growing trophozoite stage and the dormant cyst stage. Cysts are formed when the cell encounters unfavorable conditions, such as environmental stress or food deprivation. Due to their rigid double-layered wall, Acanthamoeba cysts are highly resistant to antiamoebic drugs. This is problematic as cysts can survive initially successful chemotherapeutic treatment and cause relapse of the disease. We studied the Acanthamoeba encystment process by using two-dimensional gel electrophoresis (2DE) and found that most changes in the protein content occur early in the process. Truncated actin isoforms were found to abound in the encysting cell, and the levels of translation elongation factor 2 (EF2) were sharply decreased, indicating that the rate of protein synthesis must be low at this stage. In the advanced stage of encystment, however, EF2 levels and the trophozoite proteome were partly restored. The protease inhibitors PMSF (phenylmethylsulfonyl fluoride) and E64d [(2S,3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane ethyl ester] inhibited the onset of encystment, whereas the protein synthesis inhibitor cycloheximide was ineffective. Changes in the protein profile, similar to those of encysting cells, could be observed with trophozoite homogenates incubated at room temperature for several hours. Interestingly, these changes could be inhibited significantly by cysteine protease inhibitors but not by inhibitors against other proteases. Taken together, we conclude that the encystment process in A. castellanii is of a bipartite nature consisting of an initial phase of autolysis and protein degradation and an advanced stage of restoration accompanied by the expression of encystment-specific genes.
卡氏棘阿米巴是一种兼性病原体,具有两个阶段的生命周期,包括营养生长的滋养体阶段和休眠的包囊阶段。当细胞遇到不利条件,如环境压力或食物匮乏时,就会形成包囊。由于其坚硬的双层壁,卡氏棘阿米巴包囊对抗阿米巴药物具有高度抗性。这是个问题,因为包囊可以在最初成功的化疗后存活下来并导致疾病复发。我们通过二维凝胶电泳(2DE)研究了卡氏棘阿米巴的包囊形成过程,发现蛋白质含量的大多数变化发生在该过程的早期。发现截短的肌动蛋白异构体在包囊化细胞中大量存在,而翻译延伸因子2(EF2)的水平急剧下降,表明该阶段蛋白质合成速率一定很低。然而,在包囊化的后期,EF2水平和滋养体蛋白质组部分恢复。蛋白酶抑制剂苯甲基磺酰氟(PMSF)和E64d [(2S,3S)-反式环氧琥珀酰-L-亮氨酰胺-3-甲基丁烷乙酯]抑制包囊化的开始,而蛋白质合成抑制剂环己酰亚胺无效。在室温下孵育数小时的滋养体匀浆中,可以观察到与包囊化细胞类似的蛋白质谱变化。有趣的是,这些变化可以被半胱氨酸蛋白酶抑制剂显著抑制,但不能被针对其他蛋白酶的抑制剂抑制。综上所述,我们得出结论,卡氏棘阿米巴的包囊化过程具有二分性,包括自溶和蛋白质降解的初始阶段以及伴随着包囊化特异性基因表达的恢复后期阶段。