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Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Plasmodium chabaudi chabaudi

PROVIDER: GSE132647 | GEO | 2020/04/20

REPOSITORIES: GEO

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Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 6% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.

2020-04-20 | GSE144976 | GEO

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset1]

Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 9% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.

2020-04-20 | GSE132643 | GEO

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset2]

Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 9% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.

2020-04-20 | GSE132625 | GEO

Malaria parasites regulate intra-erythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms.

Project description:Malaria parasites complete their intra-erythrocytic developmental cycle (IDC) in multiples of 24?h suggesting a circadian basis, but the mechanism controlling this periodicity is unknown. Combining in vivo and in vitro approaches utilizing rodent and human malaria parasites, we reveal that: (i) 57% of Plasmodium chabaudi genes exhibit daily rhythms in transcription; (ii) 58% of these genes lose transcriptional rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 6% of Plasmodium falciparum genes show 24?h rhythms in expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) has a 24?h transcriptional rhythm and disrupting it in rodent malaria parasites shortens the IDC by 2-3?h; (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 reveal malaria parasites are at least partly responsible for scheduling the IDC and coordinating their development with host daily rhythms.

| S-EPMC7265539 | biostudies-literature

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

Project description:Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

| PRJNA605476 | ENA

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

Project description:Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms

| PRJNA548568 | ENA

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset1]

Project description:Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset1]

| PRJNA548570 | ENA

Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset2]

Project description:Malaria parasites regulate intraerythrocytic development duration via serpentine receptor 10 to coordinate with host rhythms [Dataset2]

| PRJNA548549 | ENA

Mistimed malaria parasites re-synchronize with host feeding-fasting rhythms by shortening the duration of intra-erythrocytic development.

Project description:AimsMalaria parasites exhibit daily rhythms in the intra-erythrocytic development cycle (IDC) that underpins asexual replication in the blood. The IDC schedule is aligned with the timing of host feeding-fasting rhythms. When the IDC schedule is perturbed to become mismatched to host rhythms, it readily reschedules but it is not known how.MethodsWe intensively follow four groups of infections that have different temporal alignments between host rhythms and the IDC schedule for 10 days, before and after the peak in asexual densities. We compare how the duration, synchrony and timing of the IDC differs between parasites in control infections and those forced to reschedule by 12 hours and ask whether the density of parasites affects the rescheduling process.Results and conclusionsOur experiments reveal parasites shorten the IDC duration by 2-3 hours to become realigned to host feeding-fasting rhythms with 5-6 days, in a density-independent manner. Furthermore, parasites are able to reschedule without significant fitness costs for them or their hosts. Understanding the extent of, and limits on, plasticity in the IDC schedule may reveal targets for novel interventions, such as drugs to disrupt IDC regulation and preventing IDC dormancy conferring tolerance to existing drugs.

| S-EPMC9285586 | biostudies-literature

Malaria parasites target the hepatocyte receptor EphA2 for successful host infection.

Project description:The invasion of a suitable host hepatocyte by mosquito-transmitted Plasmodium sporozoites is an essential early step in successful malaria parasite infection. Yet precisely how sporozoites target their host cell and facilitate productive infection remains largely unknown. We found that the hepatocyte EphA2 receptor was critical for establishing a permissive intracellular replication compartment, the parasitophorous vacuole. Sporozoites productively infected hepatocytes with high EphA2 expression, and the deletion of EphA2 protected mice from liver infection. Lack of host EphA2 phenocopied the lack of the sporozoite proteins P52 and P36. Our data suggest that P36 engages EphA2, which is likely to be a key step in establishing the permissive replication compartment.

| S-EPMC4783171 | biostudies-literature

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