Tomato leaf mold is a common disease in tomato production and severely impacts the growth,fruit quality and yield of tomato plants.Research on tomato leaf mold has a long history and has focused mainly on the differen...Tomato leaf mold is a common disease in tomato production and severely impacts the growth,fruit quality and yield of tomato plants.Research on tomato leaf mold has a long history and has focused mainly on the differentiation of pathogen races,the structure and function of pathogen Avr gene products,the cloning of Cf resistance genes and the analysis of disease resistance mechanisms.Interactions between Cf and Avr are in accordance with the"gene-for-gene"hypothesis and typical Cf/Avr interactions are part of effector-triggered immunity(ETI).However,an increasing number of studies have proven that pathogen-associated molecular pattern(PAMP)-triggered immunity(PTI)is involved in the disease resistance response system mediated by Cf genes.In addition,different Cf genes have both similar and different roles in the disease resistance response,indicating that the disease resistance mechanism of Cf genes is complex.In this paper,progress in tomato leaf mold research was reviewed,and the regulatory mechanism underlying the Cf-mediated disease resistance response was thoroughly explored.We hope this summary will lay a foundation for research on tomato leaf mold disease resistance mechanisms and is applicable to breeding for disease resistance.展开更多
The abscisic acid(ABA)receptor PYR/PYL/RCAR,located upstream of the ABA signaling pathway,recognizes ABA signals and initiates the primary process of signal transduction.In our previous study,we found that the PYL4 ge...The abscisic acid(ABA)receptor PYR/PYL/RCAR,located upstream of the ABA signaling pathway,recognizes ABA signals and initiates the primary process of signal transduction.In our previous study,we found that the PYL4 gene in tomato plants was significantly upregulated after exogenous treatment with the hormone ABA.The present study used virus-induced gene silencing(VIGS)to further elucidate the role of the PYL4 gene in response to drought in tomato(Solanum lycopersicum)plants.Under the drought treatment,the SlPYL4-silenced plants wilted faster than the control plants did.Physiological indicators showed that the total reactive oxygen species(ROS)content and superoxide dismutase(SOD),peroxidase(POD)and catalase(CAT)activities of the SlPYL4-silenced plants were lower than those of the control plants after 3 and 6 h of drought stress treatment.After 3 h of drought treatment,hydrogen peroxide(H_(2)O_(2)) and superoxide anion(O_(2)^(−).)accumulatedmuch more in the leaves of the SlPYL4-silenced plants than in the leaves of the control plants.These results indicated that PYL4 plays a positive role in drought tolerance in tomato plants.Our results also suggest that SlPYL4 is located upstream of the ABA pathway to regulate the expression of PP2C,SnRK,and AREB/ABF genes.展开更多
基金supported by grants from the National Natural Science Foundation of China (Grant No.32072589)the Heilongjiang Provincial Natural Science Foundation of China (Grant No.YQ2021C013)。
文摘Tomato leaf mold is a common disease in tomato production and severely impacts the growth,fruit quality and yield of tomato plants.Research on tomato leaf mold has a long history and has focused mainly on the differentiation of pathogen races,the structure and function of pathogen Avr gene products,the cloning of Cf resistance genes and the analysis of disease resistance mechanisms.Interactions between Cf and Avr are in accordance with the"gene-for-gene"hypothesis and typical Cf/Avr interactions are part of effector-triggered immunity(ETI).However,an increasing number of studies have proven that pathogen-associated molecular pattern(PAMP)-triggered immunity(PTI)is involved in the disease resistance response system mediated by Cf genes.In addition,different Cf genes have both similar and different roles in the disease resistance response,indicating that the disease resistance mechanism of Cf genes is complex.In this paper,progress in tomato leaf mold research was reviewed,and the regulatory mechanism underlying the Cf-mediated disease resistance response was thoroughly explored.We hope this summary will lay a foundation for research on tomato leaf mold disease resistance mechanisms and is applicable to breeding for disease resistance.
基金This work was supported by the Open Project of the Key Laboratory of Biology and Genetic Improvement of Horticultural Crops(Northeast Region),Ministry of Agriculture,the National Natural Science Foundation of China(Grant No.32002059)the Heilongjiang Natural Science Foundation of China(Grant No.LH2O20C10)+1 种基金the National Key R&D Program of China(Grant No.2017YFD0101900)a fellowship from the China Postdoctoral Science Foundation(Grant No.2020M681068).
文摘The abscisic acid(ABA)receptor PYR/PYL/RCAR,located upstream of the ABA signaling pathway,recognizes ABA signals and initiates the primary process of signal transduction.In our previous study,we found that the PYL4 gene in tomato plants was significantly upregulated after exogenous treatment with the hormone ABA.The present study used virus-induced gene silencing(VIGS)to further elucidate the role of the PYL4 gene in response to drought in tomato(Solanum lycopersicum)plants.Under the drought treatment,the SlPYL4-silenced plants wilted faster than the control plants did.Physiological indicators showed that the total reactive oxygen species(ROS)content and superoxide dismutase(SOD),peroxidase(POD)and catalase(CAT)activities of the SlPYL4-silenced plants were lower than those of the control plants after 3 and 6 h of drought stress treatment.After 3 h of drought treatment,hydrogen peroxide(H_(2)O_(2)) and superoxide anion(O_(2)^(−).)accumulatedmuch more in the leaves of the SlPYL4-silenced plants than in the leaves of the control plants.These results indicated that PYL4 plays a positive role in drought tolerance in tomato plants.Our results also suggest that SlPYL4 is located upstream of the ABA pathway to regulate the expression of PP2C,SnRK,and AREB/ABF genes.