Research Training Group 2498

Research Training Group 2498

Communication and Dynamics of Plant Cell Compartments

Projects


Intercompartmental signaling of external phosphate status

Project Leader// Prof. Dr. Steffen Abel

Graduate// Pinelopi Moutesidi

Leibniz Institute of Plant Biochemistry
Department of Molecular Signal Processing
Nutrient Sensing


Phosphate (Pi) and its anhydrides are major nodes in metabolism. Thus, Pi deficiency directly impacts cellular functions and plant performance. To cope with limited Pi bioavailability, which is pervasive in many soils and caused by complex chemistries involving iron (Fe) and other metals, plants activate a set of coordinated responses to enhance Pi recycling and Pi acquisition by reprogramming metabolism and redesigning root system architecture. Pi limitation favors development of a shallow root system by attenuating primary root extension and promoting lateral root formation, adaptive growth responses thought to facilitate topsoil foraging of the immobile macronutrient. Recent studies in Arabidopsis revealed that external Pi status is monitored by growing root tips to locally inform root development. Efforts to unravel Pi sensing mechanisms are at the center of current research. To dissect local Pi sensing, we previously identified a set of Arabidopsis mutants with altered sensitivities to the root growth inhibiting effect of suboptimal Pi supply, and we characterized several PHOSPHATE DEFICIENCY RESPONSE (PDR) and LOW PHOSPHATE ROOT (LPR) genes. The encoded proteins are localized to different compartments in cells of the root apical meristem (RAM), including plastids (PDR1), the nucleus (PDR3), the ER (PDR2), endosomes (PDR4), and cell walls (LPR1, LPR2). The LPR1/PDR2 module of functionally interacting genes plays a central role and controls cell type-specific accumulation of Fe and generation of reactive oxygen species (ROS) in cell walls of the RAM. ROS-mediated callose deposition impairs cell-to-cell communication (e.g., impaired movement of transcription factors via plasmodesmata) and RAM maintenance, which causes early cell differentiation followed by root growth inhibition in limiting Pi. While LPR1 encodes a ferroxidase, PDR2 codes for the single P5-type ATPase (AtP5A) of unknown transport specificity, which likely controls LPR1 secretion or availability of LPR1 reactants. Similar as PDR2, PDR3 interacts epistatically with LPR1 but encodes a histone deacetylase subunit that represses chlorophyll synthesis and ROS production in proplastids of the RAM and proximal cortex. PDR1 (an enzyme controlling histidine and purine biosynthesis) and PDR4 (an isoprenylated heavy metal domain protein) are not focus of the proposed PhD research, but further point to intricate interactions between the nucleus, plastids, and the secretory pathway in root Pi sensing. Research in this project aims to address the following work packages:

  1. Role of non-green plastids in Pi-dependent redox signaling and callose deposition
  2. Role of JA synthesis and signaling in Pi- dependent callose deposition
  3. Impact of nuclear PDR3 on proplastid function in Pi sensing