scholarly journals Calcium‐dependent protein kinase 5 links calcium signaling with N ‐hydroxy‐ l ‐pipecolic acid‐ and SARD 1 ‐dependent immune memory in systemic acquired resistance

2019 ◽  
Vol 225 (1) ◽  
pp. 310-325 ◽  
Author(s):  
Tiziana Guerra ◽  
Silke Schilling ◽  
Katharina Hake ◽  
Karin Gorzolka ◽  
Fabian‐Philipp Sylvester ◽  
...  
2019 ◽  
Author(s):  
Tiziana Guerra ◽  
Silke Schilling ◽  
Fabian-Philipp Sylvester ◽  
Benjamin Conrads ◽  
Tina Romeis

Summary- Systemic acquired resistance (SAR) prepares infected plants for faster and stronger defense activation upon subsequent attacks. SAR requires an information relay from primary infection to distal tissue and the initiation and maintenance of a self-maintaining phytohormone salicylic acid (SA)-defense loop.- In spatial and temporal resolution we show that calcium-dependent protein kinase CPK5 contributes to immunity and SAR. In local basal resistance CPK5 functions upstream of SA-synthesis, -perception, and -signaling. In systemic tissue, enhanced CPK5 signaling leads to an accumulation of SAR marker genes including transcription factor Systemic Acquired Resistance Deficient 1 (SARD1).- Plants of enhanced CPK5-, but not CPK6-, signaling display a ‘super-priming’ phenotype of enhanced resistance toward a secondary bacterial infection. In sard1 background, CPK5-mediated basal resistance is still mounted but systemic ‘super-priming’ is lost.- The biochemical analysis determines CPK5 half maximal kinase activity for calcium K50 [Ca2+] to ∼100 nM close to the cytoplasmic resting level. This low activation threshold uniquely qualifies CPK5 to decode subtle changes in calcium prerequisite to immune signal relay and to onset and maintenance of priming at later time points in distal tissue. Our data explain why CPK5 functions as a hub in basal and systemic plant immunity.


Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4203
Author(s):  
Héloïse Débare ◽  
Nathalie Moiré ◽  
Firmin Baron ◽  
Louis Lantier ◽  
Bruno Héraut ◽  
...  

Treatments currently used to prevent congenital toxoplasmosis are non-specific of Toxoplasma gondii and have grievous side effects. To develop a more specific and less toxic drug, we have designed SP230, an imidazo[1,2-b]pyridazine salt targeting the Toxoplasma gondii calcium-dependent protein kinase 1 (TgCDPK1) and active against acute toxoplasmosis in mice. Efficiency of SP230 to inhibit foetal transmission of the parasite was evaluated in a mouse model of congenital toxoplasmosis. Swiss mice were infected at mid-pregnancy with tachyzoites or cysts of the ME49 strain of T. gondii by intraperitoneal and oral route, respectively, and treated with SP230 at 50 mg/kg for 5 days by the same routes. Parasite burden in organs of dams and in foetuses was measured by quantitative PCR. Intraperitoneal administration of SP230 drastically reduced the number of parasites (more than 97% of reduction) in the brain and lungs of dams, and led to a reduction of 66% of parasite burden in foetuses. Oral administration of SP230 was particularly efficient with 97% of reduction of parasite burdens in foetuses. SP230 did not impact number and weight of offspring in our conditions. This inhibitor of TgCDPK1 is a promising candidate for the development of alternative therapeutics to treat infected pregnant women.


PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e80818 ◽  
Author(s):  
Fei Chen ◽  
Marianna Fasoli ◽  
Giovanni Battista Tornielli ◽  
Silvia Dal Santo ◽  
Mario Pezzotti ◽  
...  

2011 ◽  
Vol 6 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Bernhard Wurzinger ◽  
Andrea Mair ◽  
Barbara Pfister ◽  
Markus Teige

BMC Genomics ◽  
2013 ◽  
Vol 14 (1) ◽  
pp. 433 ◽  
Author(s):  
Xiangpei Kong ◽  
Wei Lv ◽  
Shanshan Jiang ◽  
Dan Zhang ◽  
Guohua Cai ◽  
...  

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