When confronted with inorganic phosphate (Pi) starvation, plants activate an array of adaptive responses to sustain their growth. These responses, in a large extent, are controlled at the transcriptional level. Arabidopsis (Arabidopsis thaliana) PHOSPHATE RESPONSE1 (PHR1) and its close homolog PHR1-like 1 (PHL1) belong to a 15-member family of MYB-CC transcription factors and are regarded as the key components of the central regulatory system controlling plant transcriptional responses to Pi starvation. The knockout of PHR1 and PHL1, however, causes only a partial loss of the transcription of Pi starvation-induced genes, suggesting the existence of other key components in this regulatory system. In this work, we used the transcription of a Pi starvation-induced acid phosphatase, AtPAP10, to study the molecular mechanism underlying plant transcriptional responses to Pi starvation. We first identified a DNA sequence on the AtPAP10 promoter that is critical for the transcription of AtPAP10. We then demonstrated that PHL2 and PHL3, two other members of the MYB-CC family, specifically bind to this DNA sequence and activate the transcription of AtPAP10. Unlike PHR1 and PHL1, the transcription and protein accumulation of PHL2 and PHL3 are upregulated by Pi starvation. RNA-sequencing analyses indicated that the transcription of most Pi starvation-induced genes is impaired in the phl2 mutant, indicating that PHL2 is also a key component of the central regulatory system. Finally, we showed that PHL2, and perhaps also PHL3, acts redundantly with PHR1 to regulate plant transcriptional response to Pi starvation.

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The phytohormone ethylene plays important roles in regulating plant responses to phosphate (Pi) starvation. To date, however, no molecular components have been identified that interact with ethylene signalling in regulating such responses. In this work, an Arabidopsis mutant, hps4, was characterized that exhibits enhanced responses to Pi starvation, including increased inhibition of primary root growth, enhanced expression of Pi starvation-induced genes, and overproduction of root-associated acid phosphatases. Molecular cloning indicated that hps4 is a new allele of SABRE, which was previously identified as an important regulator of cell expansion in Arabidopsis. HPS4/SABRE antagonistically interacts with ethylene signalling to regulate plant responses to Pi starvation. Furthermore, it is shown that Pi-starved hps4 mutants accumulate more auxin in their root tips than the wild type, which may explain the increased inhibition of their primary root growth when grown under Pi deficiency.

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