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在Plasmodium中I型谷氨酸合成酶的明显演变及其特定物种的要求

Sourav Ghosh^1,2, Rajib Kundu^1,2, Manjunatha Chandana^1,3

¹Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, 751023, Odisha, India.

Nature communications

|July 14, 2023

概括

疟疾寄生虫利用一种独特的谷氨酸合成酶 (GS) 酶生存. 用MSO或PPT抑制这种必不可少的Plasmodium GS酶会破坏蛋白质合成并杀死疟疾寄生虫,包括耐药菌株.

科学领域:

生物化学生物化学
寄生虫学的寄生虫学
分子生物学分子生物学

背景情况:

疟疾寄生虫 (Plasmodium) 缺乏氨基酸生物合成途径,依赖于外部来源.
独特的谷氨酸合成酶 (GS) 基因被保留,尽管丰富的宿主谷氨酸.

研究的目的:

为了研究Plasmodium GS.的结构和调节性质.
评估作为一种抗疟疾战略的向Plasmodium GS的潜力.

主要方法:

塑菌GS作为I型酶的表征.
评估 metionin sulfoximine (MSO) 和 phosphinothricin (PPT) 对寄生虫GS的抑制作用.
在不同等离子杆菌生命阶段对GS的定位和表达分析.
调查向pfgs对阿斯巴拉金水平和蛋白质合成的影响.

主要成果:

塑菌GS表现出独特的结构和调节特征,适应无性阶段.
MSO和PPT有效地抑制了寄生虫GS活动.
向Plasmodium falciparum GS (PfGS) 破坏阿斯巴拉金的稳态,并通过eIF2α酸化抑制蛋白质合成,导致寄生虫死亡.
通过MSO/PPT抑制PfGS,可以减少活性的抗米素寄生虫的出现.

结论:

杆菌GS是一种独特的酶,对寄生虫的生存至关重要.
塑菌GS的抑制剂,如MSO和PPT,表现出强大的抗疟疾活性.
向Plasmodium GS呈现出对抗疟疾,包括耐药性感染的有希望的战略.

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