Disruption of the coordination between host circadian rhythms and malaria parasite development alters the duration of the intraerythrocytic cycle
O'Donnell, Aidan John
Abkallo, Hussein M.
Ansari, Hifzur Rahman
Abdel-Haleem, Alyaa M.
Rached, Fathia Ben
Reece, Sarah E.
KAUST DepartmentBiological and Environmental Sciences and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Pathogen Genomics Group
KAUST Grant NumberBAS/1/1020-01-01
Permanent link to this recordhttp://hdl.handle.net/10754/656930
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AbstractMalaria parasites complete their intra-erythrocytic developmental cycle (IDC) in multiples of 24 hours (depending on the species), suggesting a circadian basis to the asexual cell cycle, but the mechanism controlling this periodicity is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of Plasmodium chabaudi genes exhibit 24 h circadian periodicity in transcription; (ii) 58% of these genes lose transcriptional rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 9% of Plasmodium falciparum genes show circadian transcription under free-running conditions; (iv) Serpentine receptor 10 (SR10) has a circadian transcription profile and disrupting it in rodent malaria parasites shortens the IDC by 2-3 hours; (v) Multiple processes including DNA replication and the ubiquitin and proteasome pathways are affected by loss of coordination with host rhythms and by disruption of SR10. Our results show that malaria parasites are at least partly responsible for scheduling their IDCs explaining the fitness benefits of coordination with host rhythms.
CitationSubudhi, A. K., O’Donnell, A. J., Ramaprasad, A., Abkallo, H. M., Kaushik, A., Ansari, H. R., … Pain, A. (2019). Disruption of the coordination between host circadian rhythms and malaria parasite development alters the duration of the intraerythrocytic cycle. doi:10.1101/791046
SponsorsThe project was supported by a faculty baseline funding (BAS/1/1020-01-01) from the King Abdullah University of Science and Technology (KAUST) to AP. RC is supported by Japanese Society for the Promotion of Science (JSPS), Japan Grant-in-Aid for Scientific Research Nos. 24255009, 25870525, 16K21233 and 19K07526. SER and AJOD are supported by Wellcome (202769/Z/16/Z; 204511/Z/16/Z), the Royal Society (UF110155; NF140517) and the Human Frontier Science Program (RGP0046/2013). The authors thank the staff of the Bioscience Core Laboratory in KAUST for sequencing RNAseq libraries and all members of the Reece lab at the University of Edinburgh and pathogen genomics lab at KAUST for assistance during the experiments. This work was partly conducted at the Joint Usage / Research Center for Tropical Disease, Institute of Tropical Medicine, Nagasaki University, Japan.
PublisherCold Spring Harbor Laboratory
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