Abstract
Plants have evolved mechanisms to improve utilization efficiency or acquisition of inorganic phosphate (Pi) in response to Pi deficiency, such as altering root architecture, secreting acid phosphatases, and activating the expression of genes related to Pi uptake and recycling. Although many genes responsive to Pi starvation have been identified, transcription factors that affect tolerance to Pi deficiency have not been well characterized. We show here that the ectopic expression of B-BOX32 (BBX32) and the mutation of ELONGATED HYPOCOTYL 5 (HY5), whose transcriptional activity is negatively regulated by BBX32, resulted in the tolerance to Pi deficiency in Arabidopsis. The primary root lengths of 35S:BBX32 and hy5 plants were only slightly inhibited under Pi deficient condition and the fresh weights were significantly higher than those of wild type. The Pi deficiency-tolerant root phenotype of hy5 was similarly observed when grown on the medium without Pi. In addition, a double mutant, hy5 slr1, without lateral roots, also showed a long primary root phenotype under phosphate deficiency, indicating that the root phenotype of hy5 does not result from an increase of external Pi uptake. Moreover, we found that blue light may regulate Pi deficiency-dependent primary root growth inhibition through activating peroxidase gene expression, suggesting the Pi-deficiency tolerant root phenotype of hy5 may be due to blockage of blue light responses. Altogether, this study points out light quality may play an important role in the regulation of Pi deficiency responses. It may contribute to regulate plant growth under Pi deficiency through proper illumination.
Highlights
Inorganic phosphate (Pi) is an essential constituent of ATP, nucleic acids, and membrane phospholipids
Our results indicate that BBX32 and ELONGATED HYPOCOTYL 5 (HY5) are involved in the regulation of phosphate starvation response (PSR), and 35S:BBX32-SRDX and hy5 exhibit root tolerant phenotypes to inorganic phosphate (Pi) deficiency due to blockage of bluelight responses
The expression of INDUCED BY PHOSPHATE STARVATION1 (IPS1), RIBONUCLEASE 1 (RNS1), and ACID PHOSPHATASE TYPE 5 (ACP5) was significantly induced by Pi deficiency in the wild type (WT), but their transcript levels were much lower in 35S:BBX32-SRDX than in the WT (Figures 2B–D). These results indicate that 35S:BBX32SRDX plants appear to suffer less stress in Pi-deficient conditions compared to the WT
Summary
Inorganic phosphate (Pi) is an essential constituent of ATP, nucleic acids, and membrane phospholipids. AtPHR1 (PHOSPHATE STARVATION RESPONSE 1) is the first Arabidopsis TF gene shown to mediate diverse PSRs (Rubio et al, 2001). WRKY6 and WRKY42 negatively regulate the expression of PHOSPHATE1 (PHO1), which is responsible for Pi translocation from root to shoot in Arabidopsis (Hamburger et al, 2002; Chen et al, 2009). Several Arabidopsis TF genes, such as AtERF070, APSR1, AtMYB2, and AL6, have been shown to be involved in the regulation of root growth and architecture under Pi deficiency (Yeh and Ohme-Takagi, 2015). Proper utilization of the remaining Pi reserves is important to reduce Pi resource depletion and environmental threaten To this end, development of crops with tolerance to Pi deficiency is required, especially if crops can be manipulated to possess higher ability for Pi recycling or Pi utilization efficiency. Our results indicate that BBX32 and HY5 are involved in the regulation of PSRs, and 35S:BBX32-SRDX and hy exhibit root tolerant phenotypes to Pi deficiency due to blockage of bluelight responses
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