Adaptations in the Glucose Metabolism of Procyclic
            <i>Trypanosoma brucei</i>
            Isolates from Tsetse Flies and during Differentiation of Bloodstream Forms

Grinsven, Koen W.A. van; Abbeele, Jan Van Den; Bossche, Peter Van Den; Hellemond, Jaap J. van; Tielens, Aloysius G.M.

doi:10.1128/ec.00091-09

Cited by 36 publications

(31 citation statements)

References 25 publications

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“…L. passim was initially cultured under normoxia and migrated into the anaerobic honey bee hindgut, causing it to down-regulate the genes involved in the kinetoplast respiratory chain during middle to late stages of the infection (PI 12-27). Similar shifts in energy metabolism are also observed in other trypanosomatid parasites [41][42][43][44] . The parasites actively swim in the cultured medium using the flagellum and ATP; however, the loss of flagellum (see below) makes them immobile in the honey bee hindgut.…”

Section: Discussionsupporting

confidence: 75%

Trypanosomatid parasite dynamically changes the transcriptome during infection and modifies honey bee physiology

et al. 2020

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It is still not understood how honey bee parasite changes the gene expression to adapt to the host environment and how the host simultaneously responds to the parasite infection by modifying its own gene expression. To address this question, we studied a trypanosomatid, Lotmaria passim, which can be cultured in medium and inhabit the honey bee hindgut.We found that L. passim decreases mRNAs associated with protein translation, glycolysis, detoxification of radical oxygen species, and kinetoplast respiratory chain to adapt to the anaerobic and nutritionally poor honey bee hindgut during the infection. After the long term infection, the host appears to be in poor nutritional status, indicated by the increase and decrease of take-out and vitellogenin mRNAs, respectively. Simultaneous gene expression profiling of L. passim and honey bee during infection by dual RNA-seq provided insight into how both parasite and host modify their gene expressions.

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Section: Discussionsupporting

confidence: 75%

Trypanosomatid parasite dynamically changes the transcriptome during infection and modifies honey bee physiology

et al. 2020

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“…However, these genes appear to be down-regulated at later infection stages as the parasite switches to a dormant stage without active metabolism and proliferation. Similar shifts in energy metabolism are also observed in other trypanosomatid parasites (Bringaud et al 2006, Smith et al 2017, Van Grinsven et al 2009, van Hellemond et al 2005). Furthermore, the continuous down-regulation of tryparedoxin 1, tryparedoxin-like , and tryparedoxin peroxidase genes throughout the infection cycle is also consistent with the reduced production of radical oxygen species in anaerobic environments.…”

Section: Discussionsupporting

confidence: 77%

Honey bee trypanosomatid parasite dynamically changes the transcriptome during the infection of honey bee and modifies the host physiology

et al. 2019

Preprint

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18Although there are many honey bee pathogens/parasites, it is still not understood how 19 they change their gene expression to adapt to the host environment or how the host 20 simultaneously responds to pathogen/parasite infection by modifying its own gene 21 expression. Such interactions must lead to changes in the physiological states of both 22 host and parasite. To address this question, we studied a trypanosomatid, 23 Lotmaria passim, which can be cultured in medium and inhabit the honey bee hindgut. 24 We found that L. passim dynamically modifies the expression of mRNAs associated 25 with protein translation and the electron transport chain to adapt to the anaerobic and 26 nutritionally poor honey bee hindgut at early stages of infection, and to become dormant 27 at late stages of infection. Meanwhile, several genes are continuously up-or 28 down-regulated during infection, including GP63 as well as genes coding for host cell 29 signaling pathway modulators (up-regulated), and those involved in detoxification of 30 radical oxygen species as well as flagellar formation (down-regulated). L. passim 31 infection only slightly increases honey bee mortality and does not affect the number of 32 microorganisms in the gut microbiota; but it induces honey bee innate immune response. 33 Upon infection, the host appears to be in poor nutritional status, indicated by the 34 increase in the levels of mRNAs for take-out and facilitated trehalose transporter and 35 the decrease of vitellogenin mRNA level. Simultaneous gene expression profiling of L. 36 passim and honey bee during infection provided insight into how both parasite and host 37 modify their gene expressions. This study presents one of the best models to understand 38 host-parasite interactions at the molecular and cellular levels in honey bee. 39 40 41 42

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“…The bloodstream forms of T. brucei depend entirely on glucose metabolism through glycolysis, whose enzymes are compartmentalized in glycosomes and in turn have repressed mitochondrial activities ( 66 ). In contrast, insect forms, which need to survive in different regions of the tsetse fly’s digestive system wherein the glucose supply is irregular, rely on mitochondrial metabolism for ATP production and have sparse glycosomes ( 67 ). It has been recently shown that bloodstream forms overexpressing ATG8 proteins and incubated in a differentiation medium have a delayed transition to insect forms, as illustrated by a longer retention of glycosomes ( 68 ).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Plasmodium berghei ATG8 by Liver Forms Leads to Cumulative Defects in Organelle Dynamics and to Generation of Noninfectious Merozoites

Voss

Ehrenman

Mlambo

et al. 2016

mBio

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Plasmodium parasites undergo continuous cellular renovation to adapt to various environments in the vertebrate host and insect vector. In hepatocytes, Plasmodium berghei discards unneeded organelles for replication, such as micronemes involved in invasion. Concomitantly, intrahepatic parasites expand organelles such as the apicoplast that produce essential metabolites. We previously showed that the ATG8 conjugation system is upregulated in P. berghei liver forms and that P. berghei ATG8 (PbATG8) localizes to the membranes of the apicoplast and cytoplasmic vesicles. Here, we focus on the contribution of PbATG8 to the organellar changes that occur in intrahepatic parasites. We illustrated that micronemes colocalize with PbATG8-containing structures before expulsion from the parasite. Interference with PbATG8 function by overexpression results in poor development into late liver stages and production of small merosomes that contain immature merozoites unable to initiate a blood infection. At the cellular level, PbATG8-overexpressing P. berghei exhibits a delay in microneme compartmentalization into PbATG8-containing autophagosomes and elimination compared to parasites from the parental strain. The apicoplast, identifiable by immunostaining of the acyl carrier protein (ACP), undergoes an abnormally fast proliferation in mutant parasites. Over time, the ACP staining becomes diffuse in merosomes, indicating a collapse of the apicoplast. PbATG8 is not incorporated into the progeny of mutant parasites, in contrast to parental merozoites in which PbATG8 and ACP localize to the apicoplast. These observations reveal that Plasmodium ATG8 is a key effector in the development of merozoites by controlling microneme clearance and apicoplast proliferation and that dysregulation in ATG8 levels is detrimental for malaria infectivity.

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Adaptations in the Glucose Metabolism of Procyclic Trypanosoma brucei Isolates from Tsetse Flies and during Differentiation of Bloodstream Forms

Cited by 36 publications

References 25 publications

Trypanosomatid parasite dynamically changes the transcriptome during infection and modifies honey bee physiology

Trypanosomatid parasite dynamically changes the transcriptome during infection and modifies honey bee physiology

Honey bee trypanosomatid parasite dynamically changes the transcriptome during the infection of honey bee and modifies the host physiology

Overexpression of Plasmodium berghei ATG8 by Liver Forms Leads to Cumulative Defects in Organelle Dynamics and to Generation of Noninfectious Merozoites

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