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Studying circadian rhythms in plants and their pathogens might lead to precision medicine for people

Studying circadian rhythms in plants and their pathogens might lead to precision medicine for people | mpmi | Scoop.it
Precisely calibrated timekeepers are found in organisms from all domains of life. Biologists are studying how they influence plant/pathogen interactions – what they learn could lead to human medicines.
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Rescooped by Hua Lu from Cereal and Biotrophic Pathogens
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Tick Tock: Circadian Regulation of Plant Innate Immunity | Annual Review of Phytopathology

Many living organisms on Earth have evolved the ability to integrate environmental and internal signals to determine time and thereafter adjust appropriately their metabolism, physiology, and behavior. The circadian clock is the endogenous timekeeper critical for multiple biological processes in many organisms. A growing body of evidence supports the importance of the circadian clock for plant health. Plants activate timed defense with various strategies to anticipate daily attacks of pathogens and pests and to modulate responses to specific invaders in a time-of-day-dependent manner (gating). Pathogen infection is also known to reciprocally modulate clock activity. Such a cross talk likely reflects the adaptive nature of plants to coordinate limited resources for growth, development, and defense. This review summarizes recent progress in circadian regulation of plant innate immunity with a focus on the molecular events linking the circadian clock and defense. More and better knowledge of clock-defense cross talk could help to improve disease resistance and productivity in economically important crops.


Via IPM Lab, Wheat SAR & Lr Lab
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Rescooped by Hua Lu from Plant Immunity And Microbial Effectors
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Crosstalk between the Circadian Clock and Innate Immunity in Arabidopsis

Crosstalk between the Circadian Clock and Innate Immunity in Arabidopsis | mpmi | Scoop.it
by Chong Zhang, Qiguang Xie, Ryan G. Anderson, Gina Ng, Nicholas C. Seitz, Thomas Peterson, C. Robertson McClung, John M. McDowell, Dongdong Kong, June M.

Via IPM Lab
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Studying circadian rhythms in plants and their pathogens might lead to precision medicine for people

Studying circadian rhythms in plants and their pathogens might lead to precision medicine for people | mpmi | Scoop.it
Precisely calibrated timekeepers are found in organisms from all domains of life. Biologists are studying how they influence plant/pathogen interactions – what they learn could lead to human medicines.
more...
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Scooped by Hua Lu
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PLOS ONE: Dynamics of Defense Responses and Cell Fate Change during Arabidopsis-Pseudomonas syringae Interactions

PLOS ONE: Dynamics of Defense Responses and Cell Fate Change during Arabidopsis-Pseudomonas syringae Interactions | mpmi | Scoop.it

Plant-pathogen interactions involve sophisticated action and counteraction strategies from both parties. Plants can recognize pathogen derived molecules, such as conserved pathogen associated molecular patterns (PAMPs) and effector proteins, and subsequently activate PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), respectively. However, pathogens can evade such recognitions and suppress host immunity with effectors, causing effector-triggered susceptibility (ETS). The differences among PTI, ETS, and ETI have not been completely understood. Toward a better understanding of PTI, ETS, and ETI, we systematically examined various defense-related phenotypes of Arabidopsis infected with different Pseudomonas syringae pv. maculicola ES4326 strains, using the virulence strain DG3 to induce ETS, the avirulence strain DG34 that expresses avrRpm1 (recognized by the resistance protein RPM1) to induce ETI, and HrcC- that lacks the type three secretion system to activate PTI. We found that plants infected with different strains displayed dynamic differences in the accumulation of the defense signaling molecule salicylic acid, expression of the defense marker gene PR1, cell death formation, and accumulation/localization of the reactive oxygen species, H2O2. The differences between PTI, ETS, and ETI are dependent on the doses of the strains used. These data support the quantitative nature of PTI, ETS, and ETI and they also reveal qualitative differences between PTI, ETS, and ETI. Interestingly, we observed the induction of large cells in the infected leaves, most obviously with HrcC- at later infection stages. The enlarged cells have increased DNA content, suggesting a possible activation of endoreplication. Consistent with strong induction of abnormal cell growth by HrcC-, we found that the PTI elicitor flg22 also activates abnormal cell growth, depending on a functional flg22-receptor FLS2. Thus, our study has revealed a comprehensive picture of dynamic changes of defense phenotypes and cell fate determination during Arabidopsis-P. syringae interactions, contributing to a better understanding of plant defense mechanisms.

 

 

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Rescooped by Hua Lu from Salicylic Acid
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Salicylic Acid Regulates Plasmodesmata Closure during Innate Immune Responses in Arabidopsis

Salicylic Acid Regulates Plasmodesmata Closure during Innate Immune Responses in Arabidopsis | mpmi | Scoop.it

In plants, mounting an effective innate immune strategy against microbial pathogens involves triggering local cell death within
infected cells as well as boosting the immunity of the uninfected neighboring and systemically located cells. Although not
much is known about this, it is evident that well-coordinated cell–cell signaling is critical in this process to confine infection to
local tissue while allowing for the spread of systemic immune signals throughout the whole plant. In support of this notion,
direct cell-to-cell communication was recently found to play a crucial role in plant defense. Here, we provide experimental
evidence that salicylic acid (SA) is a critical hormonal signal that regulates cell-to-cell permeability during innate immune
responses elicited by virulent bacterial infection in Arabidopsis thaliana. We show that direct exogenous application of SA or
bacterial infection suppresses cell–cell coupling and that SA pathway mutants are impaired in this response. The SA- or
infection-induced suppression of cell–cell coupling requires an ENHANCED DESEASE RESISTANCE1– and NONEXPRESSOR
OF PATHOGENESIS-RELATED GENES1–dependent SA pathway in conjunction with the regulator of plasmodesmal gating
PLASMODESMATA-LOCATED PROTEIN5. We discuss a model wherein the SA signaling pathway and plasmodesmatamediated cell-to-cell communication converge under an intricate regulatory loop.


Via Suayib Üstün, Guogen Yang, tianxing84
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