Network nodes in the model and corresponding Boolean update rules.

<p>Network nodes in the model and corresponding Boolean update rules.</p

Attractor trees of the model for the 128 different start states.

<p>We ran the model in synchronous mode starting from each of the 128 possible combinations of states. Each circle represents a possible state of the model and the edge indicates the state to which the model evolves on the next iteration. The tree with the terminal node labelled ‘ON’ has an attractor with the same state as the steady state of runs with the model i.e GacSGacA  =  True; RpoN  =  True; HrpV  =  False; HrpG  =  True; HrpRS  =  True; HrpL  =  True; HrpA  =  True; The tree with terminal node labelled ‘OFF’ has an attractor in which all states are false.</p

States of the model at step 10 in runs with simulated knock-outs of individual genes.

<p>We ran the model in synchronous mode for 10 steps from the initial state and simulated a knock-out of a single gene, recording the model's state at step 10. Each column represents the results from a single run with a single knocked out gene, indicated above the column, each row represents a gene. Blue colour indicates that the model showed the gene was in the ‘True’ state at step 10, no colour indicates the model showed ‘False’ for the protein at step 10.</p

Network of the hrp regulon of <i>P. syringae</i>.

<p>Nodes (Blue circles) represent the proteins in the network and edges (black lines) represent regulatory interactions, arrow headed edges represent a positive regulatory interaction and T-headed edges represent a negative regulatory interaction.</p

Image2.jpeg

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p

Table3.XLSX

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p

Image3.jpeg

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p

Table1.XLSX

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p

Table6.XLSX

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p

Image6.jpeg

<p>The pathosystem of Arabidopsis thaliana and diploid biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) has been a model for investigating the molecular basis of Flor's gene-for-gene hypothesis. The isolates Hpa-Noks1 and Hpa-Cala2 are virulent on Arabidopsis accession RMX-A02 whilst an F₁ generated from a cross between these two isolates was avirulent. The F₂ progeny segregated 3,1 (avirulent, virulent), indicating a single major effect AVR locus in this pathogen. SNP-based linkage mapping confirmed a single AVR locus within a 14 kb map interval containing two genes encoding putative effectors. The Hpa-Cala2 allele of one gene, designated H. arabidopsidiscryptic1 (HAC1), encodes a protein with a signal peptide and an RxLR/dEER motif, and triggers a defense response in RMX-A02. The second gene is heterozygous in Hpa-Cala2. One allele, designated Suppressor ofHAC1^Cala2 (S-HAC1^Cala2) encodes a protein with a signal peptide and a dKEE motif with no RxLR motif; the other allele (s-hac1^Cala2) encodes a protein with a signal peptide, a dEEE motif and is divergent in sequence from the S-HAC1^Cala2 allele. In selfed progeny from Hpa-Cala2, dominant S-HAC1^Cala2 allele carrying progeny correlates with virulence in RMX-A02, whereas homozygous recessive s-hac1^Cala2 carrying progeny were avirulent. Genetic investigations suggested other heterozygous suppressor loci might exist in the Hpa-Cala2 genome.</p