Last updated 1 month ago

Disruptability [+]

Species Disruptability Reference Submitter
P. falciparum 3D7
Refractory
22127061 Theo Sanderson, Wellcome Trust Sanger Institute
P. falciparum 3D7
Refractory
18614010 Theo Sanderson, Wellcome Trust Sanger Institute
P. falciparum 3D7
Refractory
USF piggyBac screen (Insert. mut.) USF PiggyBac Screen
P. falciparum 3D7
Possible
35961464
\"Using targeted gene disruption, we show the active gene copy, PfGSK3β, is not essential for asexual blood stage proliferation, although it modulates efficient erythrocyte invasion. We found functional inactivation leads to a 69% decreased growth rate and confirmed this growth defect by rescue experiments with wild-type and catalytically inactive mutants. Functional knock-out of PfGSK3β does not lead to transcriptional up-regulation of the second copy of PfGSK3. We further analyze expression, localization, and function of PfGSK3β during gametocytogenesis using a parasite line allowing conditional induction of sexual commitment. We demonstrate PfGSK3β-deficient gametocytes show a strikingly malformed morphology leading to the death of parasites in later stages of gametocyte development. Taken together, these findings are important for our understanding and the development of PfGSK3 as an anti-malarial target.\"
Theo Sanderson, The Francis Crick Institute
P. berghei ANKA
Possible
RMgm-1219 Imported from RMgmDB
P. berghei ANKA
Refractory
RMgm-559 Imported from RMgmDB
P. berghei ANKA
Possible
PlasmoGEM (Barseq) PlasmoGEM

Mutant phenotypes [+]

Species Stage Phenotype Reference Submitter
P. falciparum 3D7 Asexual
Invasion defect
35961464
\"Using targeted gene disruption, we show the active gene copy, PfGSK3β, is not essential for asexual blood stage proliferation, although it modulates efficient erythrocyte invasion. We found functional inactivation leads to a 69% decreased growth rate and confirmed this growth defect by rescue experiments with wild-type and catalytically inactive mutants. Functional knock-out of PfGSK3β does not lead to transcriptional up-regulation of the second copy of PfGSK3. We further analyze expression, localization, and function of PfGSK3β during gametocytogenesis using a parasite line allowing conditional induction of sexual commitment. We demonstrate PfGSK3β-deficient gametocytes show a strikingly malformed morphology leading to the death of parasites in later stages of gametocyte development. Taken together, these findings are important for our understanding and the development of PfGSK3 as an anti-malarial target.\"
Theo Sanderson, The Francis Crick Institute
P. falciparum 3D7 Gametocyte
Attenuated
35961464
\"Using targeted gene disruption, we show the active gene copy, PfGSK3β, is not essential for asexual blood stage proliferation, although it modulates efficient erythrocyte invasion. We found functional inactivation leads to a 69% decreased growth rate and confirmed this growth defect by rescue experiments with wild-type and catalytically inactive mutants. Functional knock-out of PfGSK3β does not lead to transcriptional up-regulation of the second copy of PfGSK3. We further analyze expression, localization, and function of PfGSK3β during gametocytogenesis using a parasite line allowing conditional induction of sexual commitment. We demonstrate PfGSK3β-deficient gametocytes show a strikingly malformed morphology leading to the death of parasites in later stages of gametocyte development. Taken together, these findings are important for our understanding and the development of PfGSK3 as an anti-malarial target.\"
Theo Sanderson, The Francis Crick Institute
P. berghei ANKA Asexual
No difference
RMgm-1219 Imported from RMgmDB
P. berghei ANKA Asexual
No difference
PlasmoGEM (Barseq) PlasmoGEM

More information

PlasmoDB PF3D7_0312400
GeneDB PF3D7_0312400
Malaria Metabolic Pathways Localisation images
Pathways mapped to
Previous ID(s) MAL3P4.8, PFC0525c
Orthologs PBANKA_0410400 , PCHAS_0411300 , PKNH_0829800 , PVP01_0827800 , PVX_119725 , PY17X_0412900
Google Scholar Search for all mentions of this gene