TY - BOOK

T1 - Suppressing autoimmunity in Arabidopsis thaliana with dominant negative immune receptors

AU - Greeff, Michael Christiaan

PY - 2014

Y1 - 2014

N2 - A small set of Resistance proteins (R-proteins), guards plants against a large set of pathogen effector proteins that can suppress or subvert plant defense responses. The guard model attempts to solve this discrepancy by proposing that a major function of R proteins is to monitor host effector targets. In response to effector mediated changes on targets, R proteins trigger the hypersensitive response. We have proposed that a corollary to this 'guard model' is that forms of plant autoimmunity are due to inappropriate R protein activation. For example, we showed that a knockout of Accelerated Cell Death 11 (acd11) leads to inappropriate activation of hypersensitive cell death. We have previously performed a large-scale survival screen for suppressors of acd11 and found that cell death in acd11 is suppressed by mutations in a gene encoding an R protein. We have thus proposed that loss of ACD11 results in HR cell death because LAZ5 directly or indirectly guards it. The LAZ5 alleles we first found were dominant negative (laz5-DN). The laz-DN allele mutation was found in a conserved functionally important ATP binding region, the P-loop. Site-directed DN mutant alleles can be made for other R genes, as we have recently found that transgenics with similarly mutated rpm1-DN alleles lose resistance to Pseudomonas syringae expressing the AvrRpm1 effector. Accordingly, we have constructed a collection of 100 R-DN alleles and transformed them into other autoimmune mutants including camta3. CAMTA3 was previously shown to be a negative regulator of plant defense by inhibiting transcription of EDS1 and NDR1, important downstream signaling components of R-protein signaling. We found that two dominant negative alleles, DSC-D and DSC2-D, can suppress all tested camta3-1 phenotypes. We hypothesize that like acd11 and other autoimmune mutants, the increased levels of defense genes like EDS1 in camta3-1 might be a consequence of R protein activation and not merely as a result of negative regulation of plant defense responses as was previously proposed. DSC and CAMTA3 are part of a nuclear localized complex supporting the possibility that DSC is directly guarding CAMTA3.

AB - A small set of Resistance proteins (R-proteins), guards plants against a large set of pathogen effector proteins that can suppress or subvert plant defense responses. The guard model attempts to solve this discrepancy by proposing that a major function of R proteins is to monitor host effector targets. In response to effector mediated changes on targets, R proteins trigger the hypersensitive response. We have proposed that a corollary to this 'guard model' is that forms of plant autoimmunity are due to inappropriate R protein activation. For example, we showed that a knockout of Accelerated Cell Death 11 (acd11) leads to inappropriate activation of hypersensitive cell death. We have previously performed a large-scale survival screen for suppressors of acd11 and found that cell death in acd11 is suppressed by mutations in a gene encoding an R protein. We have thus proposed that loss of ACD11 results in HR cell death because LAZ5 directly or indirectly guards it. The LAZ5 alleles we first found were dominant negative (laz5-DN). The laz-DN allele mutation was found in a conserved functionally important ATP binding region, the P-loop. Site-directed DN mutant alleles can be made for other R genes, as we have recently found that transgenics with similarly mutated rpm1-DN alleles lose resistance to Pseudomonas syringae expressing the AvrRpm1 effector. Accordingly, we have constructed a collection of 100 R-DN alleles and transformed them into other autoimmune mutants including camta3. CAMTA3 was previously shown to be a negative regulator of plant defense by inhibiting transcription of EDS1 and NDR1, important downstream signaling components of R-protein signaling. We found that two dominant negative alleles, DSC-D and DSC2-D, can suppress all tested camta3-1 phenotypes. We hypothesize that like acd11 and other autoimmune mutants, the increased levels of defense genes like EDS1 in camta3-1 might be a consequence of R protein activation and not merely as a result of negative regulation of plant defense responses as was previously proposed. DSC and CAMTA3 are part of a nuclear localized complex supporting the possibility that DSC is directly guarding CAMTA3.

UR - https://soeg.kb.dk/permalink/45KBDK_KGL/fbp0ps/alma99122112762905763

M3 - Ph.D. thesis

BT - Suppressing autoimmunity in Arabidopsis thaliana with dominant negative immune receptors

PB - Department of Biology, Faculty of Science, University of Copenhagen

ER -