The plant disease triangle facing climate change: a molecular perspective.

Variations in climate conditions can dramatically affect plant health and the generation of climate-resilient crops is imperative to food security. In addition to directly affecting plants, it is predicted that more severe climate conditions will also result in greater biotic stresses. Recent studies have identified climate-sensitive molecular pathways that can result in plants being more susceptible to infection under unfavorable conditions. Here, we review how expected changes in climate will impact plant-pathogen interactions, with a focus on mechanisms regulating plant immunity and microbial virulence strategies. We highlight the complex interactions between abiotic and biotic stresses with the goal of identifying components and/or pathways that are promising targets for genetic engineering to enhance adaptation and strengthen resilience in dynamically changing environments.

Structural diversity and stress regulation of the plant immunity-associated CALMODULIN-BINDING PROTEIN 60 (CBP60) family of transcription factors in Solanum lycopersicum (tomato).

Cellular signaling generates calcium (Ca2+) ions, which are ubiquitous secondary messengers decoded by calcium-dependent protein kinases, calcineurins, calreticulin, calmodulins (CAMs), and CAM-binding proteins. Previous studies in the model plant Arabidopsis thaliana have shown the critical roles of the CAM-BINDING PROTEIN 60 (CBP60) protein family in plant growth, stress responses, and immunity. Certain CBP60 factors can regulate plant immune responses, like pattern-triggered immunity, effector-triggered immunity, and synthesis of major plant immune-activating metabolites salicylic acid (SA) and N-hydroxypipecolic acid (NHP). Although homologous CBP60 sequences have been identified in the plant kingdom, their function and regulation in most species remain unclear. In this paper, we specifically characterized 11 members of the CBP60 family in the agriculturally important crop tomato (Solanum lycopersicum). Protein sequence analyses revealed that three CBP60 homologs have the closest amino acid identity to Arabidopsis CBP60g and SARD1, master transcription factors involved in plant immunity. Strikingly, AlphaFold deep learning-assisted prediction of protein structures highlighted close structural similarity between these tomato and Arabidopsis CBP60 homologs. Conserved domain analyses revealed that they possess CAM-binding domains and DNA-binding domains, reflecting their potential involvement in linking Ca2+ signaling and transcriptional regulation in tomato plants. In terms of their gene expression profiles under biotic (Pseudomonas syringae pv. tomato DC3000 pathogen infection) and/or abiotic stress (warming temperatures), five tomato CBP60 genes were pathogen-responsive and temperature-sensitive, reminiscent of Arabidopsis CBP60g and SARD1. Overall, we present a genome-wide identification of the CBP60 gene/protein family in tomato plants, and we provide evidence on their regulation and potential function as Ca2+-sensing transcriptional regulators.

Molecular regulation of the salicylic acid hormone pathway in plants under changing environmental conditions.

Salicylic acid (SA) is a central plant hormone mediating immunity, growth, and development. Recently, studies have highlighted the sensitivity of the SA pathway to changing climatic factors and the plant microbiome. Here we summarize organizing principles and themes in the regulation of SA biosynthesis, signaling, and metabolism by changing abiotic/biotic environments, focusing on molecular nodes governing SA pathway vulnerability or resilience. We especially highlight advances in the thermosensitive mechanisms underpinning SA-mediated immunity, including differential regulation of key transcription factors (e.g., CAMTAs, CBP60g, SARD1, bHLH059), selective protein-protein interactions of the SA receptor NPR1, and dynamic phase separation of the recently identified GBPL3 biomolecular condensates. Together, these nodes form a biochemical paradigm for how the external environment impinges on the SA pathway.

The effect of the cannabinoid-receptor antagonist, SR141716, on the early stage of kainate-induced epileptogenesis in the adult rat.

Pretreatment with the endocannabinoid-receptor antagonist, SR141716, has been reported to suppress the long-lasting hyperexcitability and increased seizure susceptibility present after 30 min of hyperthermia-induced convulsions in immature rats, an animal model of complex febrile seizures in children, which may be a cause of temporal lobe epilepsy. The present experiments tested the hypothesis that SR141716 suppresses epileptogenesis in the adult kainate model, an animal model of temporal lobe epilepsy. Adult male rats (n = 35), implanted for electroencephalography (EEG) recordings, were treated with kainate. Immediately after the first acute electrographic seizure during kainate-induced status epilepticus, either vehicle or SR141716 (10 mg/kg) was injected intraperitoneally. Chronic video-EEG data were collected for the first 2-week period after kainate-induced status epilepticus. More than one-half of both the vehicle- and drug-treated animals showed spontaneous recurrent seizures. Similarly, mean seizure frequency did not differ significantly for the drug- and vehicle-treated animals during the first 2 weeks (n = 9 and 8, respectively). Therefore, no significant differences were found between SR141716-treated and control animals during the first 2 weeks of epileptogenesis. These results suggest that the endocannabinoid-receptor antagonist, SR141716, had no detectable effect on the early stages of epileptogenesis in the adult kainate model. We discuss several potential explanations for the differences in the effects of SR141716 in the adult-rat, kainate versus immature-rat, hyperthermia models.

Chronic social stress and susceptibility to concentrated ambient fine particles in rats.

BACKGROUND: Epidemiologic evidence suggests that chronic stress may alter susceptibility to air pollution. However, persistent spatial confounding between these exposures may limit the utility of epidemiologic methods to disentangle these effects and cannot identify physiologic mechanisms for potential differential susceptibilities. OBJECTIVES: Using a rat model of social stress, we compared respiratory responses to fine concentrated ambient particles (CAPs) and examined biological markers of inflammation. METHODS: Twenty-four 12-week-old male Sprague-Dawley rats were randomly assigned to four groups [stress/CAPs, stress/filtered air (FA), nonstress/CAPs, nonstress/FA]. Stress-group animals were individually introduced into the home cage of a dominant male twice weekly. Blood drawn at sacrifice was analyzed for immune and inflammatory markers. CAPs were generated using the Harvard ambient particle concentrator, which draws real-time urban ambient fine particles, enriching concentrations approximately 30 times. CAPs/FA exposures were delivered in single-animal plethysmographs, 5 hr/day for 10 days, and respiratory function was continuously monitored using a Buxco system. RESULTS: Stressed animals displayed higher average C-reactive protein, tumor necrosis factor-alpha, and white blood cell counts than did nonstressed animals. Only among stressed animals were CAPs exposures associated with increased respiratory frequency, lower flows, and lower volumes, suggesting a rapid, shallow breathing pattern. Conversely, in animals with elevated CAPs exposures alone, we observed increased inspiratory flows and greater minute volumes (volume of air inhaled or exhaled per minute). CONCLUSIONS: CAPs effects on respiratory measures differed significantly, and substantively, by stress group. Higher CAPs exposures were associated with a rapid, shallow breathing pattern only under chronic stress. Blood measures provided evidence of inflammatory responses. Results support epidemiologic findings that chronic stress may alter respiratory response to air pollution and may help elucidate pathways for differential susceptibility.

Analysis of theta power in hippocampal EEG during bar pressing and running behavior in rats during distinct behavioral contexts.

These experiments examine changes in theta power as measured by wavelet analysis in five rats performing a conditional visual discrimination task and a simple running task. In the conditional task, rats were trained to press one lever to initiate a trial and then to press one of two choice levers, each corresponding to one of two cue lights. Analysis of theta power in this operant task found a large decrease in theta power during the choice bar presses, in contrast to the increase in theta power during trial initiation bar presses. This result seems to stand counter to results that propose consistent relationships between motor actions and theta power (Vanderwolf, EEG Clin Neurophys 26:407-418, 1969), as well as studies suggesting that the lack of bar-press theta is the result of habituation. However, these data can be seen as being in broad agreement with the theoretical framework of sensorimotor integration (Bland and Oddie, Behav Brain Res 127:119-136, 2001). To investigate further the power of theta observed at the termination of type 1 motor activity, a runway task was devised in which rats ran back and forth between two ends of a linear track, one of which was always rewarded and the other never rewarded. Theta power decreased sharply 240 ms before movement ended at the rewarded end, but not at the unrewarded end of the track. These data extend the current scope of theory in demonstrating that hippocampal theta activity can end abruptly 200-400 ms prior to the end of type 1 motor movement when approaching the end of a motor sequence.

Stimulation in hippocampal region CA1 in behaving rats yields long-term potentiation when delivered to the peak of theta and long-term depression when delivered to the trough.

Experimental evidence suggests that the hippocampal theta rhythm plays a critical role in learning. Previous studies have shown long-term potentiation (LTP) to be preferentially induced with stimulation on the peak of local theta rhythm in region CA1 in anesthetized rats and with stimulation of the perforant path at the peak of theta in both anesthetized and behaving animals. We set out to determine the effects of tetanic burst stimulation in stratum radiatum of region CA1 in awake behaving animals, delivered during either the peak or the trough of the theta rhythm in the EEG. Bursts delivered to the peak resulted in an increase of 17.9 +/- 0.94% in potential slope. When identical stimulation bursts were delivered to the trough of local theta waves, the potential slope decreased 12.9 +/- 1.03%. This is the first report of LTP being preferentially induced at the peak of local theta rhythm in behaving animals in region CA1 and that LTD was found in response to tetanic stimulation at the trough of the local theta wave. The results are discussed within the framework of a recent theory that proposes that the theta rhythm sets the dynamics for alternating phases of encoding and retrieval (Hasselmo et al., 20021).