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A choline-releasing glycerophosphodiesterase essential for phosphatidylcholine biosynthesis and blood stage development in the malaria parasite

ABSTRACT: Nanopore sequencing of GDPD-null malaria parasite mutants

PROVIDER: PRJEB55180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10113962.fastq.gz	Fastqsanger.gz
	ERR10113963.fastq.gz	Fastqsanger.gz
	ERR10113964.fastq.gz	Fastqsanger.gz
	ERR10113965.fastq.gz	Fastqsanger.gz
	ERR10113966.fastq.gz	Fastqsanger.gz

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A choline-releasing glycerophosphodiesterase essential for phosphatidylcholine biosynthesis and blood stage development in the malaria parasite.

Project description:The malaria parasite Plasmodium falciparum synthesizes significant amounts of phospholipids to meet the demands of replication within red blood cells. De novo phosphatidylcholine (PC) biosynthesis via the Kennedy pathway is essential, requiring choline that is primarily sourced from host serum lysophosphatidylcholine (lysoPC). LysoPC also acts as an environmental sensor to regulate parasite sexual differentiation. Despite these critical roles for host lysoPC, the enzyme(s) involved in its breakdown to free choline for PC synthesis are unknown. Here, we show that a parasite glycerophosphodiesterase (PfGDPD) is indispensable for blood stage parasite proliferation. Exogenous choline rescues growth of PfGDPD-null parasites, directly linking PfGDPD function to choline incorporation. Genetic ablation of PfGDPD reduces choline uptake from lysoPC, resulting in depletion of several PC species in the parasite, whilst purified PfGDPD releases choline from glycerophosphocholine in vitro. Our results identify PfGDPD as a choline-releasing glycerophosphodiesterase that mediates a critical step in PC biosynthesis and parasite survival.

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Rodent malaria parasite RNA does not affect mouse BeadChip results

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Parasite and vector circadian clocks mediate efficient malaria transmission

Project description:Malaria transmission begins when Anopheles mosquitos deposit saliva and Plasmodium parasites during a bloodmeal. As Anopheles mosquitos are nocturnal, we investigated whether their salivary glands are under circadian control, anticipating bloodmeals and modulating parasite biology for host encounters. Here we show that approximately half of the mosquito salivary gland transcriptome, particularly genes essential for efficient bloodmeals such as anti-blood clotting factors, exhibits circadian expression. Furthermore, measuring hemoglobin levels, we demonstrate that mosquitos prefer to feed and ingest more blood at nighttime. Notably, we show a substantial subset of the salivary gland-resident parasite transcriptome cycling throughout the day, indicating that this stage is not transcriptionally quiescent. Among the sporozoite genes undergoing rhythmic expression are those involved in parasite motility, potentially modulating the ability to initiate infection at different times of day. Our findings suggest a circadian tripartite relationship between the vector, parasite and mammalian host that together modulate malaria transmission.

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Expression profiling of hemocytes from Anopheles gambiae after malaria parasite infection

Project description:Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify if and to what degree circulating hemocytes have altered global expression profiles after infection with the rodent malaria parasite, Plasmodium berghei Hemocytes were isolated 24-28h after infection using the infectious EGFP-CON P. berghei strain (experiment) or an invasion-deficient, Circumsporozoite- and TRAP-related protein (CTRP) knockout strain with the same genetic background as GFP-CON (CTRPko/GFP, control).

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