ApiAP2 Gene-Network Regulates Gametocytogenesis in Plasmodium Parasites

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology Pub Date : 2022-07-19 DOI:10.1155/2022/5796578

Elvis Quansah, F. Pappoe, Jilong Shen, Miao Liu, Shijie Yang, Li Yu, Chao Zhang

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引用次数: 6

Abstract

Malaria is a mosquito-borne infectious disease, caused by unicellular Apicomplexan protozoa of the genus Plasmodium. The sexual stage of Plasmodium is one of the most fascinating aspects of the Plasmodium life cycle, yet relatively less explored until now. The production of sexually fit gametocytes through gametocytogenesis is essential to the transmission of the Plasmodium parasite into an anopheline mosquito vector. Understanding how gametocytogenesis is regulated promotes the identification of novel drug targets and also the development of transmission-blocking vaccines that would help reduce the disease burden in endemic areas. Transcriptional regulation in Plasmodium parasites is primarily controlled by a family of twenty-seven Apicomplexan Apetela 2 (ApiAP2) genes which act in a cascade to enable the parasite to progress through its asexual replication as well as gametocytogenesis. Here, we review the latest progress made on members of the ApiAP2 family characterized as key players of the transcriptional machinery of gametocytes. Further, we will highlight the transcriptional regulation network of ApiAP2 genes at each stage of gametocytogenesis.

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ApiAP2基因网络调控疟原虫配子体细胞发生

疟疾是一种蚊子传播的传染病，由疟原虫属的单细胞Apiccomplex原生动物引起。疟原虫的性阶段是疟原虫生命周期中最迷人的方面之一，但迄今为止研究相对较少。通过配子细胞生成产生性适合的配子细胞对于疟原虫传播到按蚊载体中至关重要。了解配子细胞生成是如何调节的，有助于确定新的药物靶点，也有助于开发有助于减轻流行地区疾病负担的阻断传播的疫苗。疟原虫中的转录调控主要由27个ApiAP2基因家族控制，这些基因以级联方式发挥作用，使疟原虫能够通过无性复制和配子细胞生成进行。在此，我们回顾了ApiAP2家族成员在配子体转录机制中的最新进展。此外，我们将强调ApiAP2基因在配子细胞发生的每个阶段的转录调控网络。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.