SummaryRMgm-1130
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Successful modification | The gene/parasite could not be changed/generated by the genetic modification. |
The following genetic modifications were attempted | Gene disruption |
Number of attempts to introduce the genetic modification | Unknown |
Reference (PubMed-PMID number) | Not published (yet) |
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Parent parasite used to introduce the genetic modification | |
Rodent Malaria Parasite | P. berghei |
Parent strain/line | P. berghei ANKA |
Name parent line/clone | Not applicable |
Other information parent line | |
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Attempts to generate the mutant parasite were performed by | |
Name PI/Researcher | Santos, J; Llinas, M |
Name Group/Department | Biochemistry and Molecular Biology |
Name Institute | Penn State University |
City | Pennsylvania |
Country | US |
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Details of the target gene | |||||||||||||||||||||||||
Gene Model of Rodent Parasite | PBANKA_1205900 | ||||||||||||||||||||||||
Gene Model P. falciparum ortholog | PF3D7_1007700 | ||||||||||||||||||||||||
Gene product | AP2 domain transcription factor AP2-I | ||||||||||||||||||||||||
Gene product: Alternative name | ApiAP2; PfAP2-T (expressed in the trophozoite stage) | ||||||||||||||||||||||||
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Details of the genetic modification | |||||||||||||||||||||||||
Inducable system used | No | ||||||||||||||||||||||||
Additional remarks inducable system | |||||||||||||||||||||||||
Type of plasmid/construct used | not known | ||||||||||||||||||||||||
PlasmoGEM (Sanger) construct/vector used | No | ||||||||||||||||||||||||
Modified PlasmoGEM construct/vector used | No | ||||||||||||||||||||||||
Plasmid/construct map | |||||||||||||||||||||||||
Plasmid/construct sequence | |||||||||||||||||||||||||
Restriction sites to linearize plasmid | |||||||||||||||||||||||||
Partial or complete disruption of the gene | Unknown | ||||||||||||||||||||||||
Additional remarks partial/complete disruption | This mutant has been reported on the 2014 (25th) Annual Molecular Parasitology Meeting, Woodshole. In the abstract no data is provided on the details of the construct used in the attempts to knock-out this gene. When these unsuccessful attempts are published, additional information will be added to this mutant-entry. | ||||||||||||||||||||||||
Selectable marker used to select the mutant parasite | not known | ||||||||||||||||||||||||
Promoter of the selectable marker | not known | ||||||||||||||||||||||||
Selection (positive) procedure | not known | ||||||||||||||||||||||||
Selection (negative) procedure | not known | ||||||||||||||||||||||||
Additional remarks genetic modification | This mutant has been reported on the 2014 (25th) Annual Molecular Parasitology Meeting, Woodshole. In the abstract no data is provided on the details of the construct used in the attempts to knock-out this gene. When these unsuccessful attempts are published, additional information will be added to this mutant-entry. The unsuccessful attempts to knock-out this gene indicates that the protein is essential for blood stage development/multiplication. From the Abstract: C-terminal GFP-tagged PfAP2-T is expressed in trophozoites and localizes to the nucleus. Chromatin immunoprecipitation experiments followed by high-throughput sequencing (ChIP-seq) with PfAP2-T-GFP parasites indicate that PfAP2-T binds upstream of a number of rhoptry genes in vivo, as well as glideosome associated proteins (GAPs) and merozoite surface proteins (MSPs). Furthermore, immunoprecipitation assays followed by mass spectrometry demonstrate that PfAP2-T interacts with the protein Bromodomain 1 (BDP1), which has also recently been shown to associate with invasion genes. Attempts to disrupt either pfap2-t in P. falciparum or its orthologue in P. berghei (pbanka_120590) were unsuccessful and we have been unable to regulate protein expression via the FKBP destabilization system. | ||||||||||||||||||||||||
Additional remarks selection procedure | |||||||||||||||||||||||||
Primer information: Primers used for amplification of the target sequences
Primer information: Primers used for amplification of the target sequences
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