Successful modification | The parasite was generated by the genetic modification |
The mutant contains the following genetic modification(s) |
Gene disruption,
Introduction of a transgene
|
Reference (PubMed-PMID number) |
Reference 1 (PMID number) : 33771680 |
MR4 number |
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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 |
P. berghei ANKA cl15cy1
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Other information parent line | A reference wild type clone from the ANKA strain of P. berghei (PubMed: PMID: 17406255). |
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The mutant parasite was generated by |
Name PI/Researcher | Pradipta A, Yamamoto M |
Name Group/Department | Department of Immunoparasitology, Research Institute for Microbial Diseases |
Name Institute | Osaka University |
City | Osaka |
Country | Japan |
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Name of the mutant parasite |
RMgm number | RMgm-4988 |
Principal name | uis3(-) |
Alternative name | |
Standardized name | |
Is the mutant parasite cloned after genetic modification | Yes |
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Phenotype |
Asexual blood stage | Not different from wild type |
Gametocyte/Gamete | Not different from wild type |
Fertilization and ookinete | Not different from wild type |
Oocyst | Not different from wild type |
Sporozoite | Not different from wild type |
Liver stage | (Strongly) reduced development of liver stages |
Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of UIS3 and expresses luciferase and yellow-fluorescent protein (under control of the hsp70 promoter)
Protein (function)
UIS3 is a member of the ETRAMP family of proteins. these proteins are frequently located in the parasitophorous vacuole (of blood stages and liver stages). P. berghei UIS3 is expressed in both blood stages and in sporozoites (very high transcript levels) and liver stages
Phenotype
(Strongly) reduced development of liver stages
From the paper:
' The PV membranes (PVM) are coated with a well-known host autophagy marker LC3 and parasite-derived protein called Upregulated in infective sporozoites 3 (UIS3), which has been shown to interact with LC3 and inhibit LC3-mediated autophagic disruption at the PV. Although uis3(-) sporozoites cannot proliferate in wild-type cells, they can replicate efficiently in cells defective in autophagy due to the lack of Atg proteins such as Atg3, Atg5 and Atg7, since these Atg proteins are essential for processing of LC3.'
Evidence is presented:
' despite essential roles of Atg9 and Atg14 in autophagy, both proteins are dispensable for the restriction of uis3(-) parasite growth. Moreover, we found that cells lacking LC3 proteins are also able to restrict uis3(-) parasite growth. In sharp contrast, GABARAPs, another subfamily of mammalian Atg8, participated in suppression of uis3(-) parasite growth. Taken together, contrary to a previous model in which UIS3 avoids host LC3- and autophagy-dependent parasite elimination program, our data demonstrate a role of GABARAPs for suppression of uis3(-) parasite growth in a manner independent on autophagy'
Additional information
Other mutants |