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The dependency of cpr5-altered genes on SIM and SMR1 in Arabidopsis

ABSTRACT: In plants, effector-triggered immunity (ETI) is often associated with programmed cell death (PCD). Although the intracellular immune receptors involved in ETI have been studied extensively, how their activation leads to PCD and disease resistance is poorly understood. We found that the Arabidopsis nuclear envelope protein, CPR5 (constitutive expresser of PR genes 5), plays a crucial role in controlling cell fate in response to stress, as the cpr5 mutant exhibits spontaneous cell death and heightened immunity. A genetic screen revealed that the Cip/Kip CKIs (cyclin-dependent kinase inhibitors), SIM (siamese) and SMR1 (siamese-related 1), are essential for CPR5 signaling, as the sim smr1 double mutant fully suppressed the cpr5 phenotype. More significantly, PCD and ETI are compromised in sim smr1 even with the wild-type CPR5. 10-day-old wild type (Col-0), cpr5, sim smr1 and cpr5 sim smr1. 12 samples total. Replicates are derived from three independent biological experiments. We used microarrays to identify differentially expressed genes. We focused on those genes that were cpr5-altered (>2-fold) and SIM/SMR1-dependent.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: shui wang

PROVIDER: E-GEOD-40322 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The dependency of cpr5-altered genes on SIM and SMR1 in Arabidopsis

Project description:In plants, effector-triggered immunity (ETI) is often associated with programmed cell death (PCD). Although the intracellular immune receptors involved in ETI have been studied extensively, how their activation leads to PCD and disease resistance is poorly understood. We found that the Arabidopsis nuclear envelope protein, CPR5 (constitutive expresser of PR genes 5), plays a crucial role in controlling cell fate in response to stress, as the cpr5 mutant exhibits spontaneous cell death and heightened immunity. A genetic screen revealed that the Cip/Kip CKIs (cyclin-dependent kinase inhibitors), SIM (siamese) and SMR1 (siamese-related 1), are essential for CPR5 signaling, as the sim smr1 double mutant fully suppressed the cpr5 phenotype. More significantly, PCD and ETI are compromised in sim smr1 even with the wild-type CPR5.

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