Inhibition of primary root (PR) growth is a typical developmental response of Arabidopsis to phosphate (Pi) deficiency. Functional disruption of SIZ1, a SUMO E3 ligase, is known to enhance the Pi deficiency-induced inhibition of PR growth. The molecular mechanism of how SIZ1 regulates PR growth under Pi deficiency, however, remains unknown. SIZ1 was recently reported to partially SUMOylate STOP1, a transcription factor that functions in plant tolerance to aluminum toxicity and in plant responses to Pi deficiency by regulating the expression of ALMT1. ALMT1 encodes an aluminum-activated malate transporter, and its expression is induced by Pi deficiency. In siz1, the expression of ALMT1 is enhanced and the removal of Fe from Pi-deficient medium suppressed the siz1 mutant phenotype. In this report, we show that siz1 overaccumulates Fe in its root apoplasts, and consequently, produces more hydroxyl radicals, which are detrimental to root growth. Such physiological changes in siz1 can be completely suppressed by the mutation of STOP1 or ALMT1. Based on previously published work and the results of the current study, we propose that SIZ1 regulates Pi deficiency-mediated PR growth through modulating the accumulation of Fe and the production of hydroxyl radicals by controlling ALMT1 expression.
Keywords: ALMT1; Fe accumulation; hydroxyl radicals; phosphate deficiency response; primary root growth; siz1; stop1.