Phosphate-deficiency response: Understanding the signaling pathway

Plants show a high degree of physiological and developmental plasticity in response to changing nutritional conditions. One of the most limiting nutrients in many ecosystems is phosphorus. To cope with this condition plants have evolved complex mechanisms to recycle phosphate (Pi) and to increase its acquisition. Besides the knowledge about the structural genes involved in this response, little is known about the signal transduction pathways that sense Pi availability and integrate the Pi-deficiency response in plants. We made use of a conditional genetic screen to identify mutants that might assist in the dissection of Pi sensing. The screen was based on the facultative ability of Arabidopsis thaliana to use nucleic acids as the source of Pi. We isolated several mutant lines that showed impaired growth on media containing nucleic acids but which recovered on high Pi medium. Primary root growth, accumulation of starch and anthocyanins, and activities of ribonuclease and acid phosphatase isoenzymes at different Pi sources were evaluated. Two mutants, pdr1 and pdr2 were further characterized. Both mutations are recessive, belong to two complementation groups and map to chromosome 5. The short root mutant phenotypes are specific for Pi deficiency. Responses to Pi limitation are altered in both mutants. Steady-state mRNA levels of multiple Pi-starvation-inducible genes are reduced in Pi-starved pdr1 plants. In addition, cytokinin sensitivity is changed in pdr1 plants, and its short root phenotype in +Pi is rescued by the omission of external nitrate. We hypothesize that PDR1 encodes a regulatory component upstream of Pi-starvation inducible gene expression, which also is involved in cytokinin-mediated nitrogen signaling. The second mutant, pdr2, shows a conditional slow root growth phenotype that is independent of external nucleic acid hydrolysis but directly dependent on the available Pi concentration in the growth medium. Primary root growth and cell division in root meristems are inhibited in pdr2 plants below 0.1 mM Pi, but Pi-uptake is not affected. Thus, we hypothesize that PDR2 encodes a high affinity component of external Pi signaling and is necessary for attenuating and maintaining primary root cell division in low Pi and for adjusting root system architecture to Pi availability.