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Plants generate cells and organs throughout their life cycle. Plant cell proliferation relates to the activity of dividing meristematic cells, which subsequently differentiate in a position- and lineage-dependent manner. The events underlying the regulation of cell division and further differentiation processes are under tight control of both intrinsic and environmental parameters. Among the intrinsic factors, two groups of phytohormones, auxins and cytokinins, exhibit a combined regulatory impact on cell proliferation, as an important determinant for the totipotency of plant cells. Classical experiments demonstrated that application of both growth regulators in appropriate concentrations promotes callus formation. When the ratio between the phytohormones changes, callus cells acquire the competence to regenerate organs. Typically, a high auxin-to-cytokinin ratio promotes the formation of roots, whereas a low auxin-to-cytokinin ratio results in the regeneration of shoots. Conclusively, the concerted, proportional impact of both phytohormones functions as a determinant of plant cell proliferation; they act as cell cycle-promoting mitogens as well as morphogens that control plant organogenesis. Here, we describe PROPORZ1 (PRZ1), an Arabidopsis gene, essential for the developmental switch from cell proliferation to differentiation in response to variations in auxin and cytokinin concentrations. PRZ1 probably acts as a transcriptional adaptor protein that affects the expression of cell cycle regulators and might, thereby, mediate its effect on the control of cell proliferation.

The biosynthesis of plant cell wall polysaccharides requires the concerted action of nucleotide sugar interconversion enzymes, nucleotide sugar transporters, and glycosyl transferases. How cell wall synthesis in planta is regulated, however, remains unclear. The root epidermal bulger 1 (reb1) mutant in Arabidopsis thaliana is partially deficient in cell wall arabinogalactan-protein (AGP), indicating a role for REB1 in AGP biosynthesis. We show that REB1 is allelic to ROOT HAIR DEFICIENT 1 (RHD1), one of five ubiquitously expressed genes that encode isoforms of UDP-D-glucose 4-epimerase (UGE), an enzyme that acts in the formation of UDP-D-galactose (UDP-D-Gal). The RHD1 isoform is specifically required for the galactosylation of xyloglucan (XG) and type II arabinogalactan (AGII) but is not involved either in D-galactose detoxification or in galactolipid biosynthesis. Epidermal cell walls in the root expansion zone lack arabinosylated (1-->6)-beta-D-galactan and galactosylated XG. In cortical cells of rhd1, galactosylated XG is absent, but an arabinosylated (1-->6)-beta-D-galactan is present. We conclude that the flux of galactose from UDP-D-Gal into different downstream products is compartmentalized at the level of cytosolic UGE isoforms. This suggests that substrate channeling plays a role in the regulation of plant cell wall biosynthesis.

The auxin efflux carrier EIR1 (also known as AGR and AtPIN2) is a key mediator of the response of Arabidopsis roots to gravity [1,2]. This response is thought to require the establishment of a transient auxin gradient in the root meristem, resulting in differential cell elongation [3]. Recent reports suggest that EIR1 is essential for the asymmetric distribution of auxin in the root meristem [4-7], but the regulatory aspects of this process are still not fully understood. Here, we studied the regulation of EIR1 in Arabidopsis using two reporters: one was a translational fusion that contained the entire EIR1 coding sequence, and the other a transcriptional fusion that had no EIR1 coding sequence. We found that EIR1 is controlled at the post-transcriptional level. The translational fusion was unstable in response to changes in auxin homeostasis, and was destabilized by cycloheximide. In contrast, the protein was stabilized in the axr1-3 mutant, which is auxin resistant and defective in auxin responses such as root gravitropism [8,9]. AXR1 is thought to participate in ubiquitin-mediated control of protein stability [10-12]. The dependence of EIR1 reporter expression on auxin concentrations and AXR1 suggests that auxin transport is regulated through a feedback regulatory loop that affects protein stability in response to auxin.