Tellier Géraldine, Lenne Astrid, Cailliau-Maggio Katia, Cabezas-Cruz Alejandro, Valdés James J, Martoriati Alain, Aliouat El M, Gosset Pierre, Delaire Baptiste, Fréville Aline, Pierrot Christine, Khalife Jamal
Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, CHU Lille, Institut Pasteur de Lille, U1019 - UMR 8204 - Centre d'Infection et d'Immunité de Lille, Université de Lille Lille, France.
Centre National de la Recherche Scientifique, UMR 8576 - Unité de Glycobiologie Structurale et Fonctionnelle, Université de Lille Lille, France.
Front Microbiol. 2016 May 26;7:777. doi: 10.3389/fmicb.2016.00777. eCollection 2016.
Protein phosphatase 1 (PP1c) is one of the main phosphatases whose function is shaped by many regulators to confer a specific location and a selective function for this enzyme. Here, we report that eukaryotic initiation factor 2β of Plasmodium falciparum (PfeIF2β) is an interactor of PfPP1c. Sequence analysis of PfeIF2β revealed a deletion of 111 amino acids when compared to its human counterpart and the presence of two potential binding motifs to PfPP1 ((29)FGEKKK(34), (103)KVAW(106)). As expected, we showed that PfeIF2β binds PfeIF2γ and PfeIF5, confirming its canonical interaction with partners of the translation complex. Studies of the PfeIF2β-PfPP1 interaction using wild-type, single and double mutated versions of PfeIF2β revealed that both binding motifs are critical. We next showed that PfeIF2β is able to induce Germinal Vesicle Break Down (GVBD) when expressed in Xenopus oocytes, an indicator of its capacity to regulate PP1. Only combined mutations of both binding motifs abolished the interaction with PP1 and the induction of GVBD. In P. falciparum, although the locus is accessible for genetic manipulation, PfeIF2β seems to play an essential role in intraerythrocytic cycle as no viable knockout parasites were detectable. Interestingly, as for PfPP1, the subcellular fractionation of P. falciparum localized PfeIF2β in cytoplasm and nuclear extracts, suggesting a potential effect on PfPP1 in both compartments and raising the question of a non-canonical function of PfeIf2β in the nucleus. Hence, the role played by PfeIF2β in blood stage parasites could occur at multiple levels involving the binding to proteins of the translational complex and to PfPP1.
蛋白磷酸酶1(PP1c)是主要的磷酸酶之一,其功能由许多调节因子塑造,赋予该酶特定的定位和选择性功能。在此,我们报道恶性疟原虫的真核起始因子2β(PfeIF2β)是PfPP1c的相互作用蛋白。与人类对应物相比,PfeIF2β的序列分析显示缺失111个氨基酸,并且存在两个与PfPP1的潜在结合基序((29)FGEKKK(34),(103)KVAW(106))。正如预期的那样,我们表明PfeIF2β与PfeIF2γ和PfeIF5结合,证实了其与翻译复合物伙伴的典型相互作用。使用野生型、单突变和双突变版本的PfeIF2β对PfeIF2β-PfPP1相互作用的研究表明,两个结合基序都至关重要。接下来我们表明,当在非洲爪蟾卵母细胞中表达时,PfeIF2β能够诱导生发泡破裂(GVBD),这是其调节PP1能力的一个指标。只有两个结合基序的联合突变才消除了与PP1的相互作用以及GVBD的诱导。在恶性疟原虫中,尽管该基因座可用于基因操作,但PfeIF2β似乎在红细胞内周期中起重要作用,因为未检测到存活的基因敲除寄生虫。有趣的是,与PfPP1一样,恶性疟原虫的亚细胞分级分离将PfeIF2β定位在细胞质和核提取物中,这表明在两个区室中对PfPP1都有潜在影响,并提出了PfeIf2β在细胞核中的非典型功能问题。因此,PfeIF2β在血液阶段寄生虫中所起的作用可能发生在多个层面,涉及与翻译复合物蛋白和PfPP1的结合。