scholarly journals Transcription of the apicoplast genome

2016 ◽  
Vol 210 (1-2) ◽  
pp. 5-9 ◽  
Author(s):  
R.E.R. Nisbet ◽  
J.L. McKenzie
Keyword(s):  
Author(s):  
Sergio A Muñoz-Gómez ◽  
Keira Durnin ◽  
Laura Eme ◽  
Christopher Paight ◽  
Christopher E Lane ◽  
...  

Abstract A most interesting exception within the parasitic Apicomplexa is Nephromyces, an extracellular, probably mutualistic, endosymbiont found living inside molgulid ascidian tunicates (i.e., sea squirts). Even though Nephromyces is now known to be an apicomplexan, many other questions about its nature remain unanswered. To gain further insights into the biology and evolutionary history of this unusual apicomplexan, we aimed to (1) find the precise phylogenetic position of Nephromyces within the Apicomplexa, (2) search for the apicoplast genome of Nephromyces, and (3) infer the major metabolic pathways in the apicoplast of Nephromyces. To do this, we sequenced a metagenome and a metatranscriptome from the molgulid renal sac, the specialized habitat where Nephromyces thrives. Our phylogenetic analyses of conserved nucleus-encoded genes robustly suggest that Nephromyces is a novel lineage sister to the Hematozoa, which comprises both the Haemosporidia (e.g., Plasmodium) and the Piroplasmida (e.g., Babesia and Theileria). Furthermore, a survey of the renal sac metagenome revealed 13 small contigs that closely resemble the genomes of the non-photosynthetic reduced plastids, or apicoplasts, of other apicomplexans. We show that these apicoplast genomes correspond to a diverse set of most closely related but genetically divergent Nephromyces lineages that co-inhabit a single tunicate host. In addition, the apicoplast of Nephromyces appears to have retained all biosynthetic pathways inferred to have been ancestral to parasitic apicomplexans. Our results shed light on the evolutionary history of the only probably mutualistic apicomplexan known, Nephromyces, and provide context for a better understanding of its life style and intricate symbiosis.


2010 ◽  
Vol 75 (4) ◽  
pp. 942-956 ◽  
Author(s):  
Ambrish Kumar ◽  
Aiman Tanveer ◽  
Subir Biswas ◽  
Edupuganti V. S. Raghu Ram ◽  
Ankit Gupta ◽  
...  
Keyword(s):  

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e107939 ◽  
Author(s):  
Aprajita Garg ◽  
Anna Stein ◽  
William Zhao ◽  
Ankit Dwivedi ◽  
Roger Frutos ◽  
...  

2019 ◽  
Author(s):  
Víctor Hugo Jarquín-Díaz ◽  
Alice Balard ◽  
Jenny Jost ◽  
Julia Kraft ◽  
Mert Naci Dikmen ◽  
...  

AbstractDetection and quantification of coccidia in studies of wildlife can be challenging. Therefore, the prevalence of coccidia is often not assessed at the parasite species level in non-livestock animals. Parasite species-specific prevalences are especially important when studying evolutionary questions in wild populations. We tested whether increased host population density increases the prevalence of individual Eimeria species at the farm level, as predicted by epidemiological theory. We studied free-living commensal populations of the house mouse (Mus musculus) in Germany and established a strategy to detect and quantify Eimeria infections. We show that a novel diagnostic primer targeting the apicoplast genome (Ap5) and coprological assessment after flotation provide complementary detection results increasing sensitivity. Genotyping PCRs confirm detection in a subset of samples and cross-validation of different PCR markers does not indicate a bias towards a particular parasite species in genotyping. We were able to detect double infections and to determine the preferred niche of each parasite species along the distal-proximal axis of the intestine. Parasite genotyping from tissue samples provides an additional indication for the absence of species bias in genotyping amplifications. Three Eimeria species were found infecting house mice at different prevalences: Eimeria ferrisi (16.7%; 95% CI 13.2 – 20.7), E. falciformis (4.2%; 95% CI 2.6 – 6.8) and E. vermiformis (1.9%; 95% CI 0.9 – 3.8). We also find that mice in dense populations are more likely to be infected with E. falciformis and E. ferrisi.We provide methods for the assessment of prevalences of coccidia at the species level in rodent systems. We show and discuss how such data can help to test hypotheses in ecology, evolution and epidemiology on a species level.


Gene ◽  
2010 ◽  
Vol 450 (1-2) ◽  
pp. 32-38 ◽  
Author(s):  
Hideya Mitsui ◽  
Nobuko Arisue ◽  
Naoko Sakihama ◽  
Yuji Inagaki ◽  
Toshihiro Horii ◽  
...  

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Yuan Huang ◽  
Lan He ◽  
Jinfang Hu ◽  
Pei He ◽  
Junwei He ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Sabna Cheemadan ◽  
Ramya Ramadoss ◽  
Zbynek Bozdech

Calcium is a universal second messenger that plays an important role in regulatory processes in eukaryotic cells. To understand calcium-dependent signaling in malaria parasites, we analyzed transcriptional responses ofPlasmodium falciparumto two calcium ionophores (A23187 and ionomycin) that cause redistribution of intracellular calcium within the cytoplasm. While ionomycin induced a specific transcriptional response defined by up- or downregulation of a narrow set of genes, A23187 caused a developmental arrest in the schizont stage. In addition, we observed a dramatic decrease of mRNA levels of the transcripts encoded by the apicoplast genome during the exposure ofP. falciparumto both calcium ionophores. Neither of the ionophores caused any disruptions to the DNA replication or the overall apicoplast morphology. This suggests that the mRNA downregulation reflects direct inhibition of the apicoplast gene transcription. Next, we identify a nuclear encoded protein with a calcium binding domain (EF-hand) that is localized to the apicoplast. Overexpression of this protein (termed PfACBP1) inP. falciparumcells mediates an increased resistance to the ionophores which suggests its role in calcium-dependent signaling within the apicoplast. Our data indicate that theP. falciparumapicoplast requires calcium-dependent signaling that involves a novel protein PfACBP1.


Author(s):  
SooNee Tan ◽  
Devaraja G. Mudeppa ◽  
Sreekanth Kokkonda ◽  
John White ◽  
Rapatbhorn Patrapuvich ◽  
...  

Malaria parasites have three genomes: a nuclear genome, a mitochondrial genome, and an apicoplast genome. Since the apicoplast is a plastid organelle of prokaryotic origin and has no counterpart in the human host, it can be a source of novel targets for antimalarials. Plasmodium falciparum DNA gyrase ( Pf Gyr) A and B subunits both have apicoplast-targeting signals. First, to test the predicted localization of this enzyme in the apicoplast and the breadth of its function at the subcellular level, nuclear encoded Pf GyrA was disrupted using CRISPR/Cas9 gene-editing. Isopentenyl pyrophosphate (IPP) is known to rescue parasites from apicoplast inhibitors. Indeed, successful growth and characterization of Pf ΔGyrA was possible in the presence of IPP. Pf GyrA disruption was accompanied by loss of plastid acyl-carrier protein (ACP) immunofluorescence and the plastid genome. Second, ciprofloxacin, an antibacterial gyrase inhibitor, has been used for malaria prophylaxis but there is a need for a more detailed description of the mode-of-action of ciprofloxacin in malaria parasites. As predicted Pf ΔGyrA clone supplemented with IPP was less sensitive to ciprofloxacin, but not the nuclear topoisomerase inhibitor etoposide. At high concentrations, however, ciprofloxacin continued to inhibit IPP-rescued Pf ΔGyrA possibly suggesting that ciprofloxacin may have an additional non-apicoplast target in P. falciparum . Overall, we confirm that Pf GyrA is an apicoplast enzyme in the malaria parasite, essential for blood-stage parasites, and a possible target of ciprofloxacin but perhaps not the only target.


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