Redox homeostasis controls meristem activation

In the root meristemlessl (rmll) mutant, the embryonic root develops normally, but a failure to initiate cell division during germination results in seedlings with an extremely short root unable to establish and maintain an active meris-tematic zone of cell division (Cheng et al., 1995; Vernoux et al., 2000). RML1 has been found to be allelic to CADMIUM SENSITIVE2, encoding the first enzyme in the glutathione (GSH) biosynthesis pathway, 7 -glutamylcysteine synthetase (Cobbett et al., 1998; Vernoux et al., 2000). Treatment of rmll mutants with applied GSH is sufficient to restore postembryonic root development, indicating that the absence of cell division in the rml1 root results from GSH depletion (Vernoux et al., 2000). In wild-type plants, inhibiting

GSH biosynthesis has an effect on the mitotic root growth similar to that in rmll, while exogenous application increases the number of meristematic cells going through the mitotic cycle (Sanchez-Fernandez et al., 1997; Vernoux et al., 2000). Accordingly, treatment of cultured tobacco (Nicotiana tabacum) cells with the GSH biosynthesis inhibitor, buthionine sulfoximine, traps the cells in G1 phase (Vernoux et al., 2000). A role for endogenous GSH in the control of cell proliferation is provided by the mapping of GSH levels in the root meristem. Low levels of GSH are associated with the mitotically inactive QC compared to the surrounding dividing stem cells (Sanchez-Fernandez et al., 1997; Jiang et al., 2003). The glutathione redox couple GSH (reduced form) and GSSG (oxidized form) act as a homeostatic redox buffer (for a review, see Meyer and Hell, 2005). In recent years, it has become evident that the intracel-lular redox state plays a critical role in regulating cell proliferation, possibly by controlling the key components of the G1-to-S transition (den Boer and Murray, 2000; Jiang and Feldman, 2005 and references therein). Therefore, the impairment of GSH production in rmll mutants leads presumably to an overall changed redox state in the root, arresting the cells in the G1/S phase (Vernoux et al., 2000). Exactly how redox homeostasis and cell cycle regulation interconnect at the molecular level is unclear. Interestingly, auxin has been linked to changes in intracellular redox state via its correlation with the production of reactive oxygen species. Possibly, auxin contributes to the quiescence of the QC cells by maintaining these cells in the G1/S phase through redox control (Jiang et al., 2003; Jiang and Feldman, 2005).

At the moment, it is still debated whether cell cycle progression is activated before or after radicle protrusion, but early activated core cell cycle genes, such as CYCD, and the formation of a proper microtubule network certainly play the key roles in regulating the extent of cell division (Barroco et al., 2005; Masubelele et al., 2005).

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