Identification and expression analysis of twelve members of the nucleobase-ascorbate transporter (NAT) gene family in Arabidopsis thaliana

• Published in: Plant and cell physiology Vol. 47; no. 10; pp. 1381 - 1393
• Main Authors: Maurino, V.G.(Universitaet zu Koeln, Cologne (Germany)), Grube, E, Zielinski, J, Schild, A, Fischer, K, Fluegge, U.I
• Format: Journal Article
• Language: English
• Published: Japan Oxford Publishing Limited (England) 01.10.2006
• Subjects: AGALLAS; AGROBACTERIUM TUMEFACIENS; Arabidopsis - genetics; Arabidopsis Proteins - genetics; ARABIDOPSIS THALIANA; Ascorbic Acid - genetics; Ascorbic Acid - metabolism; Base Sequence; CARTE GENETIQUE; Evolution, Molecular; GALLE; Gene Expression Regulation, Plant; GENETIC MAPS; Genome, Plant; MAPAS GENETICOS; Molecular Sequence Data; Multigene Family; Nucleobase Transport Proteins - genetics; Nucleobase Transport Proteins - metabolism; Oryza sativa; Phylogeny; PLANT GALLS; TRANSPORT; TRANSPORTE; Up-Regulation
• ISSN: 0032-0781; 1471-9053
• DOI: 10.1093/pcp/pcl011

By screening genome databases, 12 genes encoding membrane proteins homologous to nucleobase-ascorbate transporters (NATs) were identified in Arabidopsis thaliana. A similar number of genes was found in the rice genome. The plant NAT proteins split into five clades (I-V) based on protein multisequence alignments. This classification nicely correlates with the patterns of organ- and tissue-specific expression during the whole life cycle of A. thaliana. Interestingly, expression of two members of clade III, AtNAT7 and AtNAT8, was found to be up-regulated in undifferentiated tissues such as callus or tumors produced by Agrobacterium tumefaciens. Clade V comprises AtNAT12 possessing a hydrophilic N-terminal extension. Transient expression of green fluorescent protein (GFP) fusions in different systems showed that AtNAT12 along with AtNAT7 and -8 are located in the plasma membrane. Mutations in any of the AtNAT genes do not induce phenotypic alterations. The absence of obvious mutant phenotypes in single but also in double and triple mutants suggests a high degree of functional redundancy between AtNAT genes, but might also point to redundant functions provided by genes or pathways unrelated to the AtNATs.