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ABSTRACT: PRL1 and FIP1 regulate plant immunity downstream of CPR5

PROVIDER: PRJNA737003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14792863_1.fastq.gz	Fastqsanger.gz
	SRR14792863_2.fastq.gz	Fastqsanger.gz
	SRR14792864_1.fastq.gz	Fastqsanger.gz
	SRR14792864_2.fastq.gz	Fastqsanger.gz
	SRR14792865_1.fastq.gz	Fastqsanger.gz

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XPO4 negatively regulates immune activation in the cpr5 mutant

Project description:Purpose: To understand the severe phenotype caused by the genetic interaction between CPR5 and XPO4, we performed the whole genome transcriptome analysis on 10-day-old seedlings of WT, xpo4, cpr5, and xpo4cpr5. Conclusions: XPO4 is a critical negative regulator of plant immunity, which is required to prevent an otherwise catastrophic induction of immune and cell death responses in the cpr5 mutant.

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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. 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.

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Project description:Identification of early transcriptional responses to CPR5 function loss in Arabidopsis Expression of CPR5 C terminal half efficiently interferes with native CPR5 protein function and causes a dominant negative effect. Four-week-old leaves of Col-0 WT and transgenic Dex:YFP-CPR5-C plant were sprayed with water or 50 uM dexamethasone to induce expression of CPR5-C. Samples were collected at 24 hours after treatment. Three biological replicates were performed per genotype per treatment.

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The polyadenylation factor FIP1 is important for plant development and root responses to abiotic stresses

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