Open AccessMon2 is a negative regulator of the monomeric G protein, Arl1
Author(s) -
Manlandro Cara Marie A.,
Palanivel Vikram R.,
Schorr Emily B.,
Mihatov Nino,
Antony Andrew A.,
Rosenwald Anne G.
Publication year - 2012
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2012.00814.x
Subject(s) - biology , phenotype , mutant , genetics , gene
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. These results are consistent with a model in which Arl1 has three different conformations in vivo . We also explored the relationship between ARL1 and MON2 using the synthetic lethal phenotype exhibited by these two genes and demonstrated that MON2 is a negative regulator of the GTP ‐restricted allele of ARL1 , ARL1[Q72L] . Finally, we constructed several new alleles predicted to alter binding of Arl1 to the sole GRIP domain containing protein in yeast, Imh1, and found that ARL1[F52G] and ARL1[Y82G] were unable to complement the loss of ARL1 with respect to either the membrane traffic or K + homeostasis phenotypes. Our study expands understanding of the roles of Arl1 in vivo .