the alveolin imc1h is required for normal ookinete and sporozoite motility behaviour and host colonisation in plasmodium berghei正常需要的alveolin imc1h动合子和孢子体能动性行为和主机在鼠体内定殖.pdfVIP

the alveolin imc1h is required for normal ookinete and sporozoite motility behaviour and host colonisation in plasmodium berghei正常需要的alveolin imc1h动合子和孢子体能动性行为和主机在鼠体内定殖.pdf

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the alveolin imc1h is required for normal ookinete and sporozoite motility behaviour and host colonisation in plasmodium berghei正常需要的alveolin imc1h动合子和孢子体能动性行为和主机在鼠体内定殖

The Alveolin IMC1h Is Required for Normal Ookinete and Sporozoite Motility Behaviour and Host Colonisation in Plasmodium berghei 1 1 1 1 1 Katrin Volkmann , Claudia Pfander , Charlotte Burstroem , Malika Ahras , David Goulding , 1 2 1 1 Julian C. Rayner , Friedrich Frischknecht , Oliver Billker *, Mathieu Brochet * 1The Wellcome Trust Sanger Institute, Hinxton, United Kingdom, 2 Department of Parasitology, Hygiene Institute, University of Heidelberg Medical School, Heidelberg, Germany Abstract Alveolins, or inner membrane complex (IMC) proteins, are components of the subpellicular network that forms a structural part of the pellicle of malaria parasites. In Plasmodium berghei, deletions of three alveolins, IMC1a, b, and h, each resulted in reduced mechanical strength and gliding velocity of ookinetes or sporozoites. Using time lapse imaging, we show here that deletion of IMC1h (PBANKA_143660) also has an impact on the directionality and motility behaviour of both ookinetes and sporozoites. Despite their marked motility defects, sporozoites lacking IMC1h were able to invade mosquito salivary glands, allowing us to investigate the role of IMC1h in colonisation of the mammalian host. We show that IMC1h is essential for sporozoites to progress through the dermis in vivo but does not play a significant role in hepatoma cell transmigration and invasion in vitro. Colocalisation of IMC1h with the residual IMC in liver stages was detected up to 30 hours after infection and parasites lacking IMC1h showed developmental defects in vitro and a delayed onset of blood stage infection in vivo. Together, these results suggest that IMC1h is involved in

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