Disruption of the C-terminal region of EBA-175 in the Dd2/Nm clone of Plasmodium falciparum does not affect erythrocyte invasion
Disruption of the C-terminal region of EBA-175 in the Dd2/Nm clone of Plasmodium falciparum does not affect erythrocyte invasion
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DOI：
10.1016/s0166-6851(00)00263-2
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发表时间：
2000-09-01
影响因子：
1.5
通讯作者：
Miller, LH
中科院分区：
文献类型：
--
作者：
Kaneko, O;Fidock, DA;Miller, LH
EBA-175是恶性疟原虫的一种微丝蛋白，与唾液酸结合在血糖蛋白A的多肽骨架上，与唾液酸依赖的红细胞侵袭有关。恶性疟原虫克隆DD2/Nm可以入侵唾液酸耗竭的红细胞，这一发现表明存在另一种入侵途径。为了研究EBA-175在这一替代途径中的作用，我们产生了表达截短形式的EBA-175的DD2/Nm克隆，该克隆缺少第6区和细胞质结构域。该蛋白似乎仍然定位于微线体附近的顶端，表明区域6和细胞质结构域不参与EBA-175向微线体的运输。在这些转基因克隆中，截短的EBA-175蛋白表达水平大大降低。EBA-175破坏的克隆显示未经处理和酶处理的人和动物红细胞的正常侵袭率，表明EBA-175在这一替代侵袭途径中缺乏参与。(C)2000年，爱思唯尔科学公司出版。
EBA-175 is a Plasmodium falciparum micronemal protein that binds to sialic acid in the context of the peptide backbone of glycophorin A and has been implicated in sialic acid-dependent invasion of erythrocytes. The existence of an alternative invasion pathway has been suggested by the finding that the P. falciparum clone Dd2/Nm can invade sialic acid-depleted erythrocytes. To study the role of EBA-175 in this alternative pathway, we have generated Dd2/Nm clones expressing a truncated form of EBA-175 that lacks region 6 and the cytoplasmic domain. The protein still appears to be localized to the apical end in the vicinity of the micronemes, suggesting that region 6 and the cytoplasmic domain are not involved in EBA-175 trafficking to the micronemes. In these genetically modified clones, the level of truncated EBA-175 protein expression was greatly reduced. EBA-175-disrupted clones displayed normal rates of invasion of untreated and enzyme-treated human and animal erythrocytes, suggesting a lack of involvement of EBA-175 in this alternative invasion pathway. (C) 2000 Published by Elsevier Science B.V.