Phosphate

Arabidopsis responds to phosphate starvation with a complex adaptive growth response. Initially, this involves a rapid inhibition of cell expansion in roots (Lai et al. 2007; Sanchez-Calderon et al. 2005; Williamson et al. 2001) and stimulation of lateral root initiation and emergence (Lopez-Bucio et al. 2002; Williamson et al. 2001). Prolonged starvation involves progressively reduced cell division, quiescence, and differentiation of cells in the apical meristem (Lai et al. 2007; Sanchez-Calderon et al. 2005; Ticconi et al. 2004). While the sequence of these events appears invariant, their kinetics and severity are quite variable between experiments and laboratories, possibly because it is very difficult to completely remove traces of phosphate from the growth media. This sequence of events implies that signaling networks involved in controlling responses to phosphate starvation target more than one of the fundamental mechanisms regulating organ growth.

Recent work indicates that the timing of onset, rate of progression, and severity of growth responses to phosphate depletion depends on the overall growth activity of the plant. Under phosphate starvation conditions, root growth is promoted by sugars and inhibited by nitrate, osmotic stress, or treatments with plant growth regulators (Lai et al. 2007). The emerging concept is that the scale of organ growth activity determines the level of demand for phosphate, which in turn influences the rate at which the plant goes through the series of adaptive growth responses.

The targets of phosphate signaling pathways involved in controlling cell growth, division, or expansion have not yet been identified. However, muta-tional dissection of adaptive responses to phosphate starvation has resulted in the identification of two interesting classes of mutants: the pdr (phosphate deficiency response) and the Ipi (low phosphate insensitive) mutants. The pdr2 mutant is hypersensitive to low phosphate availability and shows a short root phenotype under these conditions that is caused by inhibition of cell expan sion and division (Ticconi et al. 2004). The onset of quiescence and terminal differentiation observed in wild-type plants only upon extended phosphate starvation (Sanchez-Calderon et al. 2005), occurs earlier and at higher external phosphate levels, and also leads to cell death. This suggests that PDR2 might be involved in phosphate sensing or coupling perception to root growth responses.

The Ipi mutants show the opposite phenotype: these mutants are hyposensitive to phosphate starvation. Four complementation groups have been identified, all of which continue root apical growth in the absence of phosphate (Sanchez-Calderon et al. 2006). However, this is not because these plants do not know that they are experiencing phosphate starvation: these mutants activate physiological and gene expression responses to phosphate starvation to a very similar degree as wild-type (Sanchez-Calderon et al. 2006). The Ipi mutants have constitutively slightly reduced cell expansion, but dramatically increased cell division activity when compared to the wild-type in phosphate-starved conditions. These phenotypes suggest that LPI genes are involved in restraining cell division during phosphate limitation. This would serve two complementary purposes: (i) to insure the functional integrity of the root apical meristem for the longest possible time, and (ii) possibly to direct resources to incipient lateral roots to shift the patterns of root growth in favor of increasing root surface area. The cloning of PDR and LPI genes has not yet been reported, but their identification will facilitate the identification of their targets in the growth control machinery.

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