Genome wide gene amplifications and deletions in Plasmodium falciparum

2007 ◽  
Vol 155 (1) ◽  
pp. 33-44 ◽  
Author(s):  
Ulf Ribacke ◽  
Bobo W. Mok ◽  
Valtteri Wirta ◽  
Johan Normark ◽  
Joakim Lundeberg ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Genome Wide

scholarly journals Genome-Wide Collation of the Plasmodium falciparum WDR Protein Superfamily Reveals Malarial Parasite-Specific Features

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0128507 ◽  
Author(s):  
Priyanka Chahar ◽  
Manjeri Kaushik ◽  
Sarvajeet Singh Gill ◽  
Surendra Kumar Gakhar ◽  
Natrajan Gopalan ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Malarial Parasite ◽  
Protein Superfamily ◽  
Genome Wide

scholarly journals Detection of genome-wide polymorphisms in the AT-rich Plasmodium falciparum genome using a high-density microarray

BMC Genomics ◽  
2008 ◽  
Vol 9 (1) ◽  
pp. 398 ◽  
Author(s):  
Hongying Jiang ◽  
Ming Yi ◽  
Jianbing Mu ◽  
Louie Zhang ◽  
Al Ivens ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
High Density ◽  
Falciparum Genome ◽  
Genome Wide

CA/C1 peptidases of the malaria parasites Plasmodium falciparum and P. berghei and their mammalian hosts – a bioinformatical analysis

2009 ◽  
Vol 390 (11) ◽  
Author(s):  
Ke Xiao ◽  
Franz Jehle ◽  
Christoph Peters ◽  
Thomas Reinheckel ◽  
R. Heiner Schirmer ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Gene Locus ◽  
Regulatory Elements ◽  
Malaria Parasites ◽  
Mrna Regulation ◽  
Genome Wide ◽  
Bioinformatical Analysis ◽  
Genes Encoding ◽  
Rna Motif ◽  
Medical Interest

Abstract In genome-wide screens we studied CA/C1 peptidases of malaria-causing plasmodia and their hosts (man and mouse). For Plasmodium falciparum and P. berghei, several new CA/C1 peptidase genes encoding proteases of the L- and B-family with specific promoter modules were identified. In addition, two new human CA/C1 peptidase loci and one new mouse gene locus were found; otherwise, the sets of CA/C1 peptidase genes in man and mouse seem to be complete now. In each species studied there is a multitude of CA/C1 peptidases with lysosomal localization signals and partial functional overlap according to similar but subfamily-specific structures. Individual target structures in plasmodia include residues specifically different in CA/C1 peptidase subsite 2. This is of medical interest considering CA/C1 peptidase inhibition for chemotherapy in malaria, malignancies and other diseases. Promoter structures and mRNA regulation differ widely among CA/C1 peptidase subfamilies and between mammals and plasmodia. We characterized promoter modules conserved in mouse and man for the CA/C1 peptidase families B and L (with the L-like subfamily, F-like subfamily and mouse-specific J-like subfamily). RNA motif searches revealed conserved regulatory elements such as GAIT elements; plasmodial CA/C1 peptidase mRNA elements include ARE elements and mammalian mRNAs contain 15-lox DICE elements.

scholarly journals A Genome Wide Association Study of Plasmodium falciparum Susceptibility to 22 Antimalarial Drugs in Kenya

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e96486 ◽  
Author(s):  
Jason P. Wendler ◽  
John Okombo ◽  
Roberto Amato ◽  
Olivo Miotto ◽  
Steven M. Kiara ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Association Study ◽  
Genome Wide Association Study ◽  
Antimalarial Drugs ◽  
Genome Wide Association ◽  
Genome Wide ◽  
A Genome

scholarly journals Whole-genome analysis of Malawian Plasmodium falciparum isolates identifies potential targets of allele-specific immunity to clinical malaria

2020 ◽  
Author(s):  
Zalak Shah ◽  
Myo T Naung ◽  
Kara A Moser ◽  
Matthew Adams ◽  
Andrea G Buchwald ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Sequence Data ◽  
Clinical Malaria ◽  
Whole Genome Sequence ◽  
Whole Genome ◽  
Whole Genome Analysis ◽  
Multiple Alleles ◽  
Vaccine Candidates ◽  
Genome Wide ◽  
Allele Specific

Individuals acquire immunity to clinical malaria after repeated Plasmodium falciparum infections. This immunity to disease is thought to reflect the acquisition of a repertoire of responses to multiple alleles in diverse parasite antigens. In previous studies, we identified polymorphic sites within individual antigens that are associated with parasite immune evasion by examining antigen allele dynamics in individuals followed longitudinally. Here we expand this approach by analyzing genome-wide polymorphisms using whole genome sequence data from 140 parasite isolates representing malaria cases from a longitudinal study in Malawi and identify 25 genes that encode likely targets of naturally acquired immunity and that should be further characterized for their potential as vaccine candidates.

scholarly journals PfGCN5, a global regulator of stress responsive genes, modulates artemisinin resistance inPlasmodium falciparum

2019 ◽  
Author(s):  
Mukul Rawat ◽  
Abhishek Kanyal ◽  
Aishwarya Sahasrabudhe ◽  
Shruthi S. Vembar ◽  
Jose-Juan Lopez-Rubio ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Plasmodium Falciparum ◽  
Stress Responses ◽  
Artemisinin Resistance ◽  
Genetic Changes ◽  
Important Target ◽  
Genome Wide ◽  
Chromatin Regulator ◽  
Stress Responsive Genes ◽  
Almost All

AbstractPlasmodium falciparumhas evolved resistance to almost all front-line drugs including artemisinins, which threatens malaria control and elimination strategies. Oxidative stress and protein damage responses have emerged as key players in the generation of artemisinin resistance. In this study, we show that PfGCN5, a histone acetyltransferase, binds to the stress responsive and multi-variant family genes in poised state and regulates their expression under stress conditions. We have also provided biochemical and cellular evidences that PfGCN5 regulates stress responsive genes by acetylation of PfAlba3. Furthermore, we show that upon artemisinin exposure, genome-wide binding sites for PfGCN5 are increased and it is directly associated with the genes implicated in artemisinin resistance generation like BiP and TRiC chaperone. Moreover, inhibition of PfGCN5 in artemisinin resistant parasites, Kelch13 mutant, K13I543T and K13C580Y (RSA∼ 25% and 6%, respectively) reverses the sensitivity of the parasites to artemisinin treatment indicating its role in drug resistance generation. Together, these findings elucidate the role of PfGCN5 as a global chromatin regulator of stress-responses with potential role in modulating artemisinin drug resistance, and identify PfGCN5 as an important target against artemisinin resistant parasites.Author SummaryMalaria parasites are constantly adapting to the drugs we used to eliminate them. Thus, when we use the drugs to kill parasites; with time, we select the parasites with the favourable genetic changes. Parasites develop various strategies to overcome exposure to the drugs by exhibiting the stress responses. The changes specific to the drug adapted parasites can be used to understand the mechanism of drug resistance generation. In this study, we have identified PfGCN5 as a global transcriptional regulator of stress responses inPlasmodium falciparum. Inhibition of PfGCN5 reverses the sensitivity of the parasites to the artemisinin drug and identify PfGCN5 as an important target against artemisinin resistant parasites.

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