Mutational loss of Arabidopsis SLOW WALKER2 results in reduced endogenous spermine concomitant with increased aluminum sensitivity

Abstract

A previously-identified Arabidopsis mutant with hypersensitivity to aluminum, als7–1 was studied further to determine the nature of the mutation and subsequently establish the biochemical basis of the increase in Al sensitivity. Physiological analysis revealed that the Al hypersensitivity phenotype is correlated with increased Al uptake and Al-dependent gene expression, indicating that als7–1 has a defect in an Al-exclusion mechanism. Cloning of the als7–1 mutation showed that it negatively affects the gene encoding the putative nucleolar localised ribosomal biogenesis factor SLOW WALKER2, which is required for normal gametogenesis and mitotic progression. Molecular analysis indicated that Al hypersensitivity in als7–1 is correlated with loss of expression of a factor required for S-adenosylmethionine recycling and reduced levels of endogenous polyamines in the mutant. Further analysis shows that Al-dependent root growth inhibition is reversed by addition of exogenous spermine, which is correlated with a significant reduction in Al uptake by spermine treated roots. Endogenous spermine likely functions to compete with Al3+ for binding to extra- and intracellular anionic sites, which suggests that increased spermine levels may be an effective means to improve root growth in Al toxic acid soil environments.