FIGURE 2.

Schematic representation of the regulatory pathways required for plant adaptation to Pi deficiency. Under low Pi nutrition conditions (left) the transcriptional activation of a set of genes necessary for Pi uptake by the roots (PHT1, PHO1), occurs through binding of the transcription factor (TF) PHOSPHATE STARVATION RESPONSE 1(PHR1) to its cis-target present in the promoter region of these genes. Under low Pi conditions, PHR1 is sumoylated by SIZ1, and this post-translational modification is likely important for PHR1 activity because Pi-deficient regulated genes are no more induced in siz1 mutant under this condition (Miura et al., 2005), although the mechanism of this regulation is unknown. Post-transcriptional regulators of Pi transporter proteins (PHT1.1, PHO1.H1) are also transcriptionally up-regulated through PHR1 activity under Pi-deficiency. Among them the miRNA miR399 negatively regulates the ubiquitin E2 conjugase PHO2 responsible of the ubiquitination of PHT1 and PHO1 proteins in order to target them for proteasome degradation. miR399-dependent inhibition of PHO2 can be titrated under high Pi through RNA mimicry via its appariement to IPS1, a non-coding RNA positively regulated by PHR1 under Pi deficiency. Under high Pi nutrition conditions (right) PHR1 target genes are transcriptionally repressed and PHO2 expression is activated promoting Pi transporters degradation. This transcriptional repression under these conditions is mediated through Pi sensing of nuclear SPX proteins which interact with PHR1 via their SPX domain in Pi-dependent manner in order to inhibit PHR1 binding to its P1BS cis-acting sequence found in the promoter region of Pi responsive genes. Green: transcripts, red: proteins, black: post-translational modifications, arrows thickness is proportional to the strength of the considered flux.