Abstract
BACKGROUND: Innate immune signaling pathways in animals and plants are regulated by mitogen-activated protein kinase (MAPK) cascades. MAP kinase 4 (MPK4) functions downstream of innate immune receptors via a nuclear substrate MKS1 to regulate the activity of the WRKY33 transcription factor, which in turn controls the production of anti-microbial phytoalexins. METHODOLOGY/PRINCIPAL FINDINGS: We investigate the role of MKS1 in basal resistance and the importance of its N- and C-terminal domains for MKS1 function. We used the information that mks1 loss-of-function partially suppresses the mpk4 loss-of-function phenotype, and that transgenic expression of functional MKS1 in mpk4/mks1 double mutants reverted the mpk4 dwarf phenotype. Transformation of mks1/mpk4 with mutant versions of MKS1 constructs showed that a single amino acid substitution in a putative MAP kinase docking domain, MKS1-L32A, or a truncated MKS1 version unable to interact with WRKY33, were deficient in reverting the double mutant to the mpk4 phenotype. These results demonstrate functional requirement in MKS1 for the interaction with MPK4 and WRKY33. In addition, nuclear localization of MKS1 was shown to depend on an intact N-terminal domain. Furthermore, loss-of-function mks1 mutants exhibited increased susceptibility to strains of Pseudomonas syringae and Hyaloperonospora arabidopsidis, indicating that MKS1 plays a role in basal defense responses. CONCLUSIONS: Taken together, our results indicate that MKS1 function and subcellular location requires an intact N-terminus important for both MPK4 and WRKY33 interactions.
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Claims 5
Claim · model-written summary
MKS1-L32A failed to restore the mpk4 phenotype in mks1/mpk4 plants.
- Taxon
- Arabidopsis
Arabidopsist0 - Material
- MKS1-L32Ae0
- Treatment
- a single amino acid substitution in a putative MAP kinase docking domain, MKS1-L32Ae0
- Gene
- MKS1-L32Ae0
- Outcome
- reverting the double mutant to the mpk4 phenotypee0
- Direction
- deficiente0
- Comparator
- mpk4 phenotypee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.

Verbatim
e0“a single amino acid substitution in a putative MAP kinase docking domain, MKS1-L32A, or a truncated MKS1 version unable to interact with WRKY33, were deficient in reverting the double mutant to the mpk4 phenotype”
t0“Arabidopsis”
Claim · model-written summary
Truncated MKS1 unable to interact with WRKY33 failed to restore the mpk4 phenotype.
- Taxon
- Arabidopsis
Arabidopsist0 - Treatment
- a truncated MKS1 version unable to interact with WRKY33e0
- Gene
- MKS1e0
- Outcome
- reverting the double mutant to the mpk4 phenotypee0
- Direction
- deficiente0
- Comparator
- mpk4 phenotypee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.

Verbatim
e0“a truncated MKS1 version unable to interact with WRKY33, were deficient in reverting the double mutant to the mpk4 phenotype”
t0“Arabidopsis”
Claim · model-written summary
MKS1 nuclear localization depended on its intact N-terminal domain.
- Taxon
- Arabidopsis
Arabidopsist0 - Gene
- MKS1e0
- Outcome
- nuclear localization of MKS1e0
- Qualifier
- an intact N-terminal domaine0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.

Verbatim
e0“nuclear localization of MKS1 was shown to depend on an intact N-terminal domain”
t0“Arabidopsis”
Claim · model-written summary
Loss of MKS1 increased susceptibility to Pseudomonas syringae.
- Taxon
- Arabidopsis
Arabidopsist0 - Material
- mks1 mutantse0
- Treatment
- loss-of-function mks1e0
- Interactor
- Pseudomonas syringae
Pseudomonas syringaee0pathogen - Gene
- mks1e0
- Outcome
- susceptibility to strains of Pseudomonas syringaee0
- Direction
- increasede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.


Verbatim
e0“loss-of-function mks1 mutants exhibited increased susceptibility to strains of Pseudomonas syringae and Hyaloperonospora arabidopsidis”
t0“Arabidopsis”
Claim · model-written summary
Loss of MKS1 increased susceptibility to Hyaloperonospora arabidopsidis.
- Taxon
- Arabidopsis
Arabidopsist0 - Material
- mks1 mutantse0
- Treatment
- loss-of-function mks1e0
- Interactor
- Hyaloperonospora arabidopsidis
Hyaloperonospora arabidopsidise0pathogen - Gene
- mks1e0
- Outcome
- susceptibility to strains of Pseudomonas syringae and Hyaloperonospora arabidopsidise0
- Direction
- increasede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.


Verbatim
e0“loss-of-function mks1 mutants exhibited increased susceptibility to strains of Pseudomonas syringae and Hyaloperonospora arabidopsidis”
t0“Arabidopsis”
The same questions in other papers
loss of function · Hyaloperonospora arabidopsidis · ArabidopsisPositive and negative results
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loss of function · Pseudomonas syringae · ArabidopsisPositive and negative results
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See all 20 papers →Claims are grouped by organism, treatment and what was measured or targeted. A paper counts as positive when any of its claims in the group is positive.