RMgmDB - Rodent Malaria genetically modified Parasites

Summary

RMgm-5273
Malaria parasiteP. yoelii
Genotype
DisruptedGene model (rodent): PY17X_1369800; Gene model (P.falciparum): PF3D7_1351300; Gene product: conserved Plasmodium membrane protein, unknown function
PhenotypeNo phenotype has been described
Last modified: 29 December 2022, 16:12
  *RMgm-5273
Successful modificationThe parasite was generated by the genetic modification
The mutant contains the following genetic modification(s) Gene disruption
Reference (PubMed-PMID number) Not published (yet)
MR4 number
Parent parasite used to introduce the genetic modification
Rodent Malaria ParasiteP. yoelii
Parent strain/lineP. y. yoelii 17XNL
Name parent line/clone Not applicable
Other information parent line
The mutant parasite was generated by
Name PI/ResearcherGoswami D, Vaughan AM
Name Group/DepartmentCenter for Global Infectious Disease Research
Name InstituteSeattle Children’s Research Institute
CitySeattle
CountryUSA
Name of the mutant parasite
RMgm numberRMgm-5273
Principal namePY17X_1369800(-)
Alternative name
Standardized name
Is the mutant parasite cloned after genetic modificationYes
Phenotype
Asexual blood stageNot different from wild type
Gametocyte/GameteNot different from wild type
Fertilization and ookineteNot different from wild type
OocystNot different from wild type
SporozoiteNot different from wild type
Liver stageNot different from wild type
Additional remarks phenotype

Mutant/mutation
The mutant lacks expression of PY17X_1369800.

No details are provided in the manuscript on the generation of this gene-deletion mutant. From the manuscript: 'Gene knockout of PY17X_1369800 was achieved but the phenotype of the knockout was equivalent to wildtype across the life cycle and thus this gene deletion was not pursued further (data not shown).

Published in: bioRxiv preprint doi: https://doi.org/10.1101/2022.12.13.519845

Protein (function)
The protein was identified by the following analysis: 'To identify novel genes that play critical roles only during liver stage development, we took advantage of a late liver stage P. vivax (Pv) transcriptome that was generated from infected livers of human-liver chimeric FRG huHep mice (manuscript in preparation). To enrich for liver stage specific reads, the Pv RPKM reads were expressed as a fold change over the maximal RPKM reads for the orthologous Pf genes expressed during the blood stage of the life cycle (manuscript in preparation). This enabled us to compare and contrast asexual Pv liver stage development with asexual Pf blood stage development and specifically identify conserved transcripts that were highly expressed only during late liver stage development. PY17X_1369800/PF3D7_1351300 belonged to the top 10 genes.

Phenotype
Normal/wildtype phenotype throughout the complete life cycle.

No details are provided in the manuscript on the generation of this gene-deletion mutant.
From the manuscript: 'Gene knockout of PY17X_1369800 was achieved but the phenotype of the knockout was equivalent to wildtype across the life cycle and thus this gene deletion was not pursued further (data not shown).

Additional information

Other mutants


  Disrupted: Mutant parasite with a disrupted gene
Details of the target gene
Gene Model of Rodent Parasite PY17X_1369800
Gene Model P. falciparum ortholog PF3D7_1351300
Gene productconserved Plasmodium membrane protein, unknown function
Gene product: Alternative name
Details of the genetic modification
Inducable system usedNo
Additional remarks inducable system
Type of plasmid/construct usedunknown
PlasmoGEM (Sanger) construct/vector usedNo
Modified PlasmoGEM construct/vector usedNo
Plasmid/construct map
Plasmid/construct sequence
Restriction sites to linearize plasmid
Partial or complete disruption of the geneComplete
Additional remarks partial/complete disruption
Selectable marker used to select the mutant parasiteunknown
Promoter of the selectable markerunknown
Selection (positive) procedureN.A
Selection (negative) procedureN.A.
Additional remarks genetic modificationNo details are provided in the manuscript on the generation of this gene-deletion mutant.
From the manuscript: 'Gene knockout of PY17X_1369800 was achieved but the phenotype of the knockout was equivalent to wildtype across the life cycle and thus this gene deletion was not pursued further (data not shown).
Additional remarks selection procedure
Primer information: Primers used for amplification of the target sequences  Click to view information
Primer information: Primers used for amplification of the target sequences  Click to hide information
Sequence Primer 1
Additional information primer 1
Sequence Primer 2
Additional information primer 2
Sequence Primer 3
Additional information primer 3
Sequence Primer 4
Additional information primer 4
Sequence Primer 5
Additional information primer 5
Sequence Primer 6
Additional information primer 6