ABSTRACT
Temperature impacts plant immunity and growth but how temperature intersects with endogenous pathways to shape natural variation remains unclear. Here we uncover variation between Arabidopsis thaliana natural accessions in response to two non-stress temperatures (22°C and 16°C) affecting accumulation of the thermoresponsive stress hormone salicylic acid (SA) and plant growth. Analysis of differentially responding A. thaliana accessions shows that pre-existing SA provides a benefit in limiting infection by Pseudomonas syringae pathovar tomato DC3000 bacteria at both temperatures. Several A. thaliana genotypes display a capacity to mitigate negative effects of high SA on growth, indicating within-species plasticity in SA-growth tradeoffs. An association study of temperature x SA variation, followed by physiological and immunity phenotyping of mutant and over-expression lines, identifies the transcription factor bHLH059 as a temperature-responsive SA immunity regulator. Here we reveal previously untapped diversity in plant responses to temperature and a way forward in understanding the genetic architecture of plant adaptation to changing environments.
Subject(s)
Arabidopsis Proteins/genetics , Arabidopsis/genetics , Plant Immunity/genetics , Thermosensing/genetics , Arabidopsis/immunology , Arabidopsis/physiology , Arabidopsis Proteins/immunology , Gene Expression Regulation, Plant/drug effects , Plant Diseases/genetics , Plant Diseases/immunology , Plant Leaves/genetics , Plant Leaves/growth & development , Pseudomonas syringae/genetics , Salicylic Acid/metabolism , Signal Transduction/drug effects , Temperature , Thermosensing/immunology , Transcription Factors/geneticsABSTRACT
The hypothesis that the early inflammatory cell, the neutrophil, contributes to the hyperalgesia resulting from peripheral nerve injury was tested in rats in which the sciatic nerve was partially transected on one side. The extent and time-course of neutrophilic infiltration of the sciatic nerve and innervated paw skin after partial nerve damage was characterized using immunocytochemistry. The number of endoneurial neutrophils was significantly elevated in sections of operated nerve compared to sections of sham-operated nerve for the entire period studied, i.e. up to seven days post-surgery. This considerable elevation in endoneurial neutrophil numbers was only observed at the site of nerve injury. Depletion of circulating neutrophils at the time of nerve injury significantly attenuated the induction of hyperalgesia. However, depletion of circulating neutrophils at day 8 post-injury did not alleviate hyperalgesia after its normal induction. It is concluded that endoneurial accumulation of neutrophils at the site of peripheral nerve injury is important in the early genesis of the resultant hyperalgesia. The findings support the notion that a neuroimmune interaction occurs as a result of peripheral nerve injury and is important in the subsequent development of neuropathic pain.
