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http://purl.uniprot.org/citations/17951519http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17951519http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17951519http://www.w3.org/2000/01/rdf-schema#comment"Ammonia has been shown to function as a morphogen at multiple steps during the development of the cellular slime mold Dictyostelium discoideum; however, it is largely unknown how intracellular ammonia levels are controlled. In the Dictyostelium genome, there are five genes that encode putative ammonium transporters: amtA, amtB, amtC, rhgA, and rhgB. Here, we show that AmtA regulates ammonia homeostasis during growth and development. We found that cells lacking amtA had increased levels of ammonia/ammonium, whereas their extracellular ammonia/ammonium levels were highly decreased. These results suggest that AmtA mediates the excretion of ammonium. In support of a role for AmtA in ammonia homeostasis, AmtA mRNA is expressed throughout the life cycle, and its expression level increases during development. Importantly, AmtA-mediated ammonia homeostasis is critical for many developmental processes. amtA(-) cells are more sensitive to NH(4)Cl than wild-type cells in inhibition of chemotaxis toward cyclic AMP and of formation of multicellular aggregates. Furthermore, even in the absence of exogenously added ammonia, we found that amtA(-) cells produced many small fruiting bodies and that the viability and germination of amtA(-) spores were dramatically compromised. Taken together, our data clearly demonstrate that AmtA regulates ammonia homeostasis and plays important roles in multiple developmental processes in Dictyostelium."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.org/dc/terms/identifier"doi:10.1128/ec.00204-07"xsd:string
http://purl.uniprot.org/citations/17951519http://purl.org/dc/terms/identifier"doi:10.1128/ec.00204-07"xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Iijima M."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Iijima M."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Kuwayama H."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Kuwayama H."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Tanaka Y."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Tanaka Y."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Yamada Y."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Yamada Y."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Morio T."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Morio T."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Sameshima M."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Sameshima M."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Yoshino R."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Yoshino R."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Sesaki H."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/author"Sesaki H."xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/name"Eukaryot. Cell"xsd:string
http://purl.uniprot.org/citations/17951519http://purl.uniprot.org/core/name"Eukaryot. Cell"xsd:string