Aluminum-Dependent Root-Growth Inhibition in Arabidopsis Results from AtATR-Regulated Cell-Cycle Arrest

• Published in: Current biology 2008-10, Vol.18 (19), p.1495-1500
• Main Authors: Rounds, Megan A., Larsen, Paul B.
• Format: Article
• Language: English
• Subjects: Aluminum - metabolism; Arabidopsis; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Ataxia Telangiectasia Mutated Proteins; Cell Cycle; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; CELLCYCLE; DNA; DNA Damage; Plant Roots - growth & development; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism
• ISSN: 0960-9822; 1879-0445
• DOI: 10.1016/j.cub.2008.08.050

Aluminum (Al) toxicity is a global problem severely limiting agricultural productivity in acid-soil regions comprising upwards of 50% of the world's arable land [1, 2]. Although Al-exclusion mechanisms have been intensively studied [3–9], little is known about tolerance to internalized Al, which is predicted to be mechanistically complex because of the plethora of predicted cellular targets for Al 3+ [2, 10]. An Arabidopsis mutant with Al hypersensitivity, als3-1, was found to represent a lesion in a phloem and root-tip-localized factor similar to the bacterial ABC transporter ybbm, with ALS3 likely responsible for Al transfer from roots to less-sensitive tissues [10–12]. To identify mutations that enhance mechanisms of Al resistance or tolerance, a suppressor screen for mutants that mask the Al hypersensitivity of als3-1 was performed [13]. Two allelic suppressors conferring increased Al tolerance were found to represent dominant-negative mutations in a factor required for monitoring DNA integrity, AtATR [14–17]. From this work, Al-dependent root-growth inhibition primarily arises from DNA damage coupled with AtATR-controlled blockage of cell-cycle progression and terminal differentiation because of loss of the root-quiescent center, with mutations that prevent response to this damage resulting in quiescent-center maintenance and sustained vigorous growth in an Al-toxic environment.