Cloned (Comment) | Organism |
---|---|
in procyclic-form parasite cells, V5-tagged KREPB9 or KREPB10 alleles are constitutively expressed from the tubulin locus in the background of the respective CN cell line in the absence of the tet-regulated expression of the wild-type allele in the rDNA locus | Trypanosoma brucei |
Protein Variants | Comment | Organism |
---|---|---|
G238R | site-directed mutagenesis of KREPB10, the mutant has reduced steady-state levels compared to wild-type KREPB10 | Trypanosoma brucei |
G238V | site-directed mutagenesis of KREPB10, the mutant has reduced steady-state levels compared to wild-type KREPB10 | Trypanosoma brucei |
G270R | site-directed mutagenesis of KREPB9, the G270R mutant protein is considerably weaker due to the lower steady-state level | Trypanosoma brucei |
G270V | site-directed mutagenesis of KREPB9, mutant does not appear to shift compared to the wild-type | Trypanosoma brucei |
additional information | generation of KREPB9 and KREPB10 null mutants. KREPB9 null cells show negligible differences in growth compared to parental 427 wild-type cells and single-knockout cells that retain KREPB9 expression. In KREPB10 null cells, growth is identical to single-knockout cells that retain KREPB10 expression, negligible differences from 427 wild-type cells | Trypanosoma brucei |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
cytoplasm | - |
Trypanosoma brucei | 5737 | - |
mitochondrion | - |
Trypanosoma brucei | 5739 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Trypanosoma brucei | Q38F97 | - |
- |
Trypanosoma brucei | Q57X12 | - |
- |
Trypanosoma brucei 927/4 GUTat10.1 | Q38F97 | - |
- |
Trypanosoma brucei 927/4 GUTat10.1 | Q57X12 | - |
- |
Synonyms | Comment | Organism |
---|---|---|
KREPB10 | - |
Trypanosoma brucei |
KREPB9 | - |
Trypanosoma brucei |
RNase III | - |
Trypanosoma brucei |
Tb09.160.3050 | - |
Trypanosoma brucei |
Tb927.8.5700 | - |
Trypanosoma brucei |
General Information | Comment | Organism |
---|---|---|
malfunction | while RNA interference (RNAi) knockdown of either KREPB9 or KREPB10 produces no growth defect in procyclic-form parasites, the extent of the knockdown is relatively weak, with only 29% of KREPB9 mRNA or 43% of KREPB10 mRNA eliminated in each cell line | Trypanosoma brucei |
metabolism | editosomes are the multiprotein complexes that catalyze the insertion and deletion of uridines to create translatable mRNAs in the mitochondria of kinetoplastids. Recognition and cleavage of a broad diversity of RNA substrates in vivo require three functionally distinct RNase III-type endonucleases (that act at distinct sites), as well as five additional editosome proteins that contain noncatalytic RNase III domains. RNase III domains have been identified in the editosome accessory proteins KREPB9 and KREPB10, suggesting a role related to editing endonuclease function, although KREPB9 and KREPB10 are not essential in either bloodstream-form parasites or procyclic-form parasites. Editosome interactions with KREPB9 and KREPB10 are mediated by the noncatalytic RNase III domain, consistent with a role in endonuclease specialization in Trypanosoma brucei. KREPB9 and KREPB10 are essential for editosome association, potentially via dimerization with RNase III domains in other editosome proteins | Trypanosoma brucei |
physiological function | importance of RNase III domain interactions to editosome architecture. Association of KREPB9 and KREPB10 with about 20S editosomes requires the RNase III structure | Trypanosoma brucei |