A holistic view on plant effector-triggered immunity presented as an iceberg model
Research output: Contribution to journal › Review › Research › peer-review
Standard
A holistic view on plant effector-triggered immunity presented as an iceberg model. / Thordal-Christensen, Hans.
In: Cellular and Molecular Life Sciences, Vol. 77, 2020, p. 3963-3976.Research output: Contribution to journal › Review › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - A holistic view on plant effector-triggered immunity presented as an iceberg model
AU - Thordal-Christensen, Hans
PY - 2020
Y1 - 2020
N2 - The immune system of plants is highly complex. It involves pattern-triggered immunity (PTI), which is signaled and manifested through branched multi-step pathways. To counteract this, pathogen effectors target and inhibit individual PTI steps. This in turn can cause specific plant cytosolic nucleotide-binding leucine-rich repeat (NLR) receptors to activate effector-triggered immunity (ETI). Plants and pathogens have many genes encoding NLRs and effectors, respectively. Yet, only a few segregate genetically as resistance (R) genes and avirulence (Avr) effector genes in wild-type populations. In an attempt to explain this contradiction, a model is proposed where far most of the NLRs, the effectors and the effector targets keep one another in a silent state. In this so-called "iceberg model", a few NLR-effector combinations are genetically visible above the surface, while the vast majority is hidden below. Besides, addressing the existence of many NLRs and effectors, the model also helps to explain why individual downregulation of many effectors causes reduced virulence and why many lesion-mimic mutants are found. Finally, the iceberg model accommodates genuine plant susceptibility factors as potential effector targets.
AB - The immune system of plants is highly complex. It involves pattern-triggered immunity (PTI), which is signaled and manifested through branched multi-step pathways. To counteract this, pathogen effectors target and inhibit individual PTI steps. This in turn can cause specific plant cytosolic nucleotide-binding leucine-rich repeat (NLR) receptors to activate effector-triggered immunity (ETI). Plants and pathogens have many genes encoding NLRs and effectors, respectively. Yet, only a few segregate genetically as resistance (R) genes and avirulence (Avr) effector genes in wild-type populations. In an attempt to explain this contradiction, a model is proposed where far most of the NLRs, the effectors and the effector targets keep one another in a silent state. In this so-called "iceberg model", a few NLR-effector combinations are genetically visible above the surface, while the vast majority is hidden below. Besides, addressing the existence of many NLRs and effectors, the model also helps to explain why individual downregulation of many effectors causes reduced virulence and why many lesion-mimic mutants are found. Finally, the iceberg model accommodates genuine plant susceptibility factors as potential effector targets.
KW - Plant immunity
KW - Pathogen effectors
KW - Nucleotide-binding leucine-rich repeat receptors
KW - Lesion mimic mutants
KW - Susceptibility
KW - RECEPTOR RESISTANCE PROTEINS
KW - POWDERY MILDEW RESISTANCE
KW - MAP KINASE CASCADE
KW - SALICYLIC-ACID
KW - PATHOGEN EFFECTORS
KW - PENETRATION RESISTANCE
KW - DEFENSE RESPONSES
KW - ARABIDOPSIS EDS1
KW - CALLOSE SYNTHASE
KW - PIPECOLIC ACID
U2 - 10.1007/s00018-020-03515-w
DO - 10.1007/s00018-020-03515-w
M3 - Review
C2 - 32277261
VL - 77
SP - 3963
EP - 3976
JO - EXS
JF - EXS
SN - 1023-294X
ER -
ID: 249477382