Publications by authors named "Cara Marie A Manlandro"
Using site-directed mutants of ARL1 predicted to alter nucleotide binding, we examined phenotypes associated with the loss of ARL1 , including effects on membrane traffic and K (+) homeostasis. The GTP-restricted allele, ARL[Q72L] , complemented the membrane traffic phenotype (CPY secretion), but not the K (+) homeostasis phenotypes (sensitivity to hygromycin B, steady-state levels of K (+) , and accumulation of (86) Rb (+) ), while the XTP-restricted mutant, ARL1[D130N] , complemented the ion phenotypes, but not the membrane traffic phenotype. A GDP-restricted allele, ARL1[T32N] , did not effectively complement either phenotype.
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- SAP155 acts as a negative modulator of potassium (K+) efflux in yeast, meaning that increasing SAP155 levels reduces K+ loss, while removing it leads to higher K+ efflux.
- SAP185, a related protein, functions oppositely by promoting K+ efflux, showing that the balance between SAP155 and SAP185 regulates K+ levels in the cell.
- Both SAP155 and SAP185 require the SIT4 protein for their activity, which plays a crucial role in the cell cycle, indicating a complex interplay between these proteins and potassium homeostasis in yeast.
Article Synopsis
- The yeast ARL1 gene is associated with a guanine-nucleotide binding protein from the Arf-like family and interacts genetically with CCZ1.
- An arl1 Delta ccz1 Delta double mutant is viable but shows slower growth and increased sensitivity to substances like caffeine and zinc, alongside more severe issues in vacuolar protein sorting.
- Overexpressing either ARL1 or CCZ1 does not alleviate the mutant phenotypes of the other, indicating that both genes play independent roles in ion homeostasis and protein sorting.