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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

An importin alpha homolog, MOS6, plays an important role in plant innate immunity.

Plant disease resistance is the consequence of an innate defense mechanism mediated by Resistance (R) genes [1]. The conserved structure of one class of R protein is reminiscent of Toll-like receptors (TLRs) and Nucleotide binding oligomerization domain (NOD) proteins-immune-response perception modules in animal cells [2, 3, and 4]. The Arabidopsis snc1 (suppressor of npr1-1, constitutive, 1) mutant contains a mutation in a TIR-NBS-LRR-type of R gene that renders resistance responses constitutively active without interaction with pathogens [5]. Few components of the downstream signaling network activated by snc1 are known. To search for regulators of R-gene-mediated resistance, we screened for genetic suppressors of snc1. Three alleles of the mutant mos6 (modifier of snc1, 6) partially suppressed constitutive-resistance responses and immunity to virulent pathogens in snc1. Furthermore, the mos6-1 single mutant exhibited enhanced disease susceptibility to a virulent oomycete pathogen. MOS6, identified by positional cloning, encodes importin alpha3, one of eight alpha importins in Arabidopsis [6]. alpha importins mediate the import of specific proteins across the nuclear envelope. We previously reported that MOS3, a protein homologous to human nucleoporin 96, is required for constitutive resistance in snc1 [7]. Our data highlight an essential role for nucleo-cytoplasmic trafficking, especially protein import, in plant innate immunity.[1]


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