| Literature DB >> 29576450 |
Shang Ma1, Stuart Cahalan1, Gregory LaMonte2, Nathan D Grubaugh3, Weizheng Zeng1, Swetha E Murthy1, Emma Paytas2, Ramya Gamini4, Viktor Lukacs1, Tess Whitwam1, Meaghan Loud1, Rakhee Lohia5, Laurence Berry5, Shahid M Khan6, Chris J Janse6, Michael Bandell7, Christian Schmedt7, Kai Wengelnik5, Andrew I Su4, Eric Honore8, Elizabeth A Winzeler2, Kristian G Andersen9, Ardem Patapoutian10.
Abstract
Hereditary xerocytosis is thought to be a rare genetic condition characterized by red blood cell (RBC) dehydration with mild hemolysis. RBC dehydration is linked to reduced Plasmodium infection in vitro; however, the role of RBC dehydration in protection against malaria in vivo is unknown. Most cases of hereditary xerocytosis are associated with gain-of-function mutations in PIEZO1, a mechanically activated ion channel. We engineered a mouse model of hereditary xerocytosis and show that Plasmodium infection fails to cause experimental cerebral malaria in these mice due to the action of Piezo1 in RBCs and in T cells. Remarkably, we identified a novel human gain-of-function PIEZO1 allele, E756del, present in a third of the African population. RBCs from individuals carrying this allele are dehydrated and display reduced Plasmodium infection in vitro. The existence of a gain-of-function PIEZO1 at such high frequencies is surprising and suggests an association with malaria resistance.Entities:
Keywords: PIEZO1; cerebral malaria; dehydration; functional variants; genomics; human genetics; ion channel; malaria; mechanotransduction; red blood cell
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Year: 2018 PMID: 29576450 PMCID: PMC5889333 DOI: 10.1016/j.cell.2018.02.047
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582