scholarly journals Metabolites of plants and their role in resistance to phytopathogens

2003 ◽  
Vol 1 (1) ◽  
pp. 47-58
Author(s):  
Ludmila A Lutova ◽  
Galina M Shumilina

Plant disease resistance is a complex reaction where biochemical peculiarities play a major role. The review is focused on two strategies of improvement of plant resistance to some groups of pathogens. The first strategy is based on a dependence of pathogens on certain plant compounds, i.e. sterols. The lack of these metabolites in a host plant repress pathogen development and reproduction. Here we present modern data on sterol metabolism and their functions in plants as well as description of known plant sterol mutants. The other way to improve plant resistance is to stimulate biosynthesis of secondary metabolites with antimicrobial activity. The roles of phytoalexins and steroid glycoalcoloids in the development of plant resistance is described here on certain examples

2021 ◽  
Author(s):  
Zhizhong Gong ◽  
Junsheng Qi ◽  
Aifang Ma ◽  
Dingpeng Zhang ◽  
Guangxing Wang ◽  
...  

Verticillium wilt is a severe plant disease, increasing the plant resistance to this disease is a critical challenge worldwide. Here, we report that the Verticillium dahliae (V. dahliae)-secreted Aspf2-like protein VDAL causes leaf wilting when applied to cotton leaves in vitro, but enhances the resistance to V. dahliae when overexpressed in Arabidopsis or cotton. VDAL interacts with Arabidopsis E3 ligases PUB25 and PUB26 (PUBs) and is ubiquitinated by PUBs in vitro. However, VDAL is not degraded by PUBs in planta. Besides, the pub25 pub26 shows higher resistance to V. dahliae than the wild type. PUBs interact with the transcription factor MYB6 in a yeast two-hybrid screen. MYB6 promotes plant resistance to Verticillium wilt while PUBs ubiquitinate MYB6 and mediate its degradation. VDAL competes with MYB6 for binding to PUBs, and the role of VDAL in increasing wilt disease depends on MYB6. These results suggest that plants evolute a strategy to utilize the invaded effector protein VDAL to resist the V. dahliae infection without causing a hypersensitive response. This study provides the molecular mechanism for plants increasing disease resistance when overexpressing some effector proteins, and may promote searching for more genes from pathogenic fungi or bacteria to engineer plant disease resistance.


2021 ◽  
Author(s):  
Aifang Ma ◽  
Dingpeng Zhang ◽  
Guangxing Wang ◽  
Kai Wang ◽  
Zhen Li ◽  
...  

Abstract Verticillium wilt is a severe plant disease that causes massive losses in multiple crops. Increasing the plant resistance to Verticillium wilt is a critical challenge worldwide. Here, we report that the hemibiotrophic Verticillium dahliae-secreted Asp f2-like protein VDAL causes leaf wilting when applied to cotton leaves in vitro but enhances the resistance to V. dahliae when overexpressed in Arabidopsis or cotton without affecting the plant growth and development. VDAL protein interacts with Arabidopsis E3 ligases plant U-box 25 (PUB25) and PUB26 and is ubiquitinated by PUBs in vitro. However, VDAL is not degraded by PUB25 or PUB26 in planta. Besides, the pub25 pub26 double mutant shows higher resistance to V. dahliae than the wild-type. PUBs interact with the transcription factor MYB6 in a yeast two-hybrid screen. MYB6 promotes plant resistance to Verticillium wilt while PUBs ubiquitinate MYB6 and mediate its degradation. VDAL competes with MYB6 for binding to PUBs, and the role of VDAL in increasing Verticillium wilt resistance depends on MYB6. Taken together, these results suggest that plants evolute a strategy to utilize the invaded effector protein VDAL to resist the V. dahliae infection without causing a hypersensitive response (HR); alternatively, hemibiotrophic pathogens may use some effectors to keep plant cells alive during its infection in order to take nutrients from host cells. This study provides the molecular mechanism for plants increasing disease resistance when overexpressing some effector proteins without inducing HR, and may promote searching for more genes from pathogenic fungi or bacteria to engineer plant disease resistance.


2021 ◽  
Vol 171 (4) ◽  
pp. 849-867
Author(s):  
Basavantraya N. Devanna ◽  
Rajdeep Jaswal ◽  
Pankaj Kumar Singh ◽  
Ritu Kapoor ◽  
Priyanka Jain ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document