BHLH32 modulates several biochemical and morphological processes that respond to P sub(i) starvation in Arabidopsis

• Published in: Biochemical journal Vol. 405; no. 1
• Main Authors: Chen, Zhi-Hui, Nimmo, Gillian A, Jenkins, Gareth I, Nimmo, Hugh G
• Format: Journal Article
• Language: English
• Published: 01-01-2007
• Subjects: Arabidopsis
• EISSN: 1470-8728
• ISSN: 0264-6021

P sub(i) (inorganic phosphate) limitation severely impairs plant growth and reduces crop yield. Hence plants have evolved several biochemical and morphological responses to P sub(i) starvation that both enhance uptake and conserve use. The mechanisms involved in P sub(i) sensing and signal transduction are not completely understood. In the present study we report that a previously uncharacterized transcription factor, BHLH32, acts as a negative regulator of a range of P sub(i) starvation-induced processes in Arabidopsis. In bhlh32 mutant plants in P sub(i)-sufficient conditions, expression of several P sub(i) starvation-induced genes, formation of anthocyanins, total P sub(i) content and root hair formation were all significantly increased compared with the wild-type. Among the genes negatively regulated by BHLH32 are those encoding PPCK (phosphoenolpyruvate carboxylase kinase), which is involved in modifying metabolism so that P sub(i) is spared. The present study has shown that PPCK genes are rapidly induced by P sub(i) starvation leading to increased phosphorylation of phosphoenolpyruvate carboxylase. Furthermore, several Arabidopsis proteins that regulate epidermal cell differentiation [TTG1 (TRANSPARENT TESTA GLABRA1), GL3 (GLABRA3) and EGL3 (ENHANCER OF GL3)] positively regulate PPCK gene expression in response to P sub(i) starvation. BHLH32 can physically interact with TTG1 and GL3. We propose that BHLH32 interferes with the function of TTG1-containing complexes and thereby affects several biochemical and morphological processes that respond to P sub(i) availability.