scholarly journals Natural Variation in Partial Resistance to Pseudomonas syringae Is Controlled by Two Major QTLs in Arabidopsis thaliana

PLoS ONE ◽  
2006 ◽  
Vol 1 (1) ◽  
pp. e123 ◽  
Author(s):  
Laure Perchepied ◽  
Thomas Kroj ◽  
Maurice Tronchet ◽  
Olivier Loudet ◽  
Dominique Roby
PLoS Genetics ◽  
2021 ◽  
Vol 17 (1) ◽  
pp. e1009290
Author(s):  
Friederike Bruessow ◽  
Jaqueline Bautor ◽  
Gesa Hoffmann ◽  
Ipek Yildiz ◽  
Jürgen Zeier ◽  
...  

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.


2010 ◽  
Vol 63 (3) ◽  
pp. 443-457 ◽  
Author(s):  
Jane L. Ward ◽  
Silvia Forcat ◽  
Manfred Beckmann ◽  
Mark Bennett ◽  
Sonia J. Miller ◽  
...  

2021 ◽  
Author(s):  
Arnaud-Thierry Djami-Tchatchou ◽  
Zipeng Alex Li ◽  
Paul Stodghill ◽  
Melanie J. Filiatrault ◽  
Barbara N. Kunkel

The auxin indole-3-acetic acid (IAA) is a plant hormone that not only regulates plant growth and development but also plays important roles in plant-microbe interactions. We previously reported that IAA alters expression of several virulence-related genes in the plant pathogen Pseudomonas syringae pv. tomato strain DC3000 ( Pto DC3000). To learn more about the impact of IAA on regulation of Pto DC3000 gene expression we performed a global transcriptomic analysis of bacteria grown in culture, in the presence or absence of exogenous IAA. We observed that IAA repressed expression of genes involved in the Type III secretion (T3S) system and motility and promoted expression of several known and putative transcriptional regulators. Several of these regulators are orthologs of factors known to regulate stress responses and accordingly expression of several stress response-related genes was also upregulated by IAA. Similar trends in expression for several genes were also observed by RT-qPCR. Using an Arabidopsis thaliana auxin receptor mutant that accumulates elevated auxin, we found that many of the P. syringae genes regulated by IAA in vitro were also regulated by auxin in planta . Collectively the data indicate that IAA modulates many aspects of Pto DC3000 biology, presumably to promote both virulence and survival under stressful conditions, including those encountered in or on plant leaves. IMPORTANCE Indole-3-acetic acid (IAA), a form of the plant hormone auxin, is used by many plant-associated bacteria as a cue to sense the plant environment. Previously, we showed that IAA can promote disease in interactions between the plant pathogen Pseudomonas syringae strain Pto DC000 and one of its hosts, Arabidopsis thaliana . However, the mechanisms by which IAA impacts the biology of Pto DC3000 and promotes disease are not well understood. Here we demonstrate that IAA is a signal molecule that regulates gene expression in Pto DC3000. The presence of exogenous IAA affects expression of over 700 genes in the bacteria, including genes involved in Type III secretion and genes involved in stress response. This work offers insight into the roles of auxin promoting pathogenesis.


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