Dataset Information


Expression data of pmr1∆ mutants

ABSTRACT: The yeast PMR1 (ATP2C1) gene codes for the eukaryotic prototype of a high affinity P-type ATPase required for Ca2+/Mn2+ transport into the Golgi. Cells lacking PMR1 exhibit multiple genetic interactions with genes involved in DNA recombination and replication, a fact that is not yet understood. We find that deletion of PMR1 causes a delay in DNA replication initiation, progression and G2/M transition and induces the transcriptional up-regulation of genes involved in cell cycle regulation, including CLB5 and SWE1. Interestingly, pmr1∆ clb5∆ double mutants exhibit a dramatic delay in DNA replication and increased DNA breakage, while endoreplication and the formation of multi-nucleated, giant yeast is observed in pmr1∆ swe1∆ cells. Because these phenotypes can be attributed to impeded Mn2+-pump function, we provide a model in which Mn2+ interferes with Mg2+ in the nucleus, and vice versa, Mg2+ interferes with Mn2+ in the Golgi. Consequently, cell cycle progression is challenged by aberrant catalytic activities of enzymes involved in replication and protein glycosylation. Three repeats of pmr1∆ mutant. Total RNA levels in pmr1∆ mutants were analyzed and compared to the wild type submitted to the GEO database under the accession number GSE29334 (C. Gonzalez-Aguilera and A. Aguilera).

ORGANISM(S): Saccharomyces cerevisiae  

SUBMITTER: Nestor Garcia-Rodriguez   Ralf E Wellinger  Néstor Garcia-Rodriguez 

PROVIDER: E-GEOD-29420 | ArrayExpress | 2012-06-17



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Impaired manganese metabolism causes mitotic misregulation.

García-Rodríguez Néstor N   Díaz de la Loza María del Carmen Mdel C   Andreson Bethany B   Monje-Casas Fernando F   Rothstein Rodney R   Wellinger Ralf Erik RE  

The Journal of biological chemistry 20120404 22

Manganese is an essential trace element, whose intracellular levels need to be carefully regulated. Mn(2+) acts as a cofactor for many enzymes and excess of Mn(2+) is toxic. Alterations in Mn(2+) homeostasis affect metabolic functions and mutations in the human Mn(2+)/Ca(2+) transporter ATP2C1 have been linked to Hailey-Hailey disease. By deletion of the yeast orthologue PMR1 we have studied the impact of Mn(2+) on cell cycle progression and show that an excess of cytosolic Mn(2+) alters S-phase  ...[more]

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