Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA292160 | ENA |
REPOSITORIES: ENA
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Project description:Plant-parasitic cyst nematodes induce the formation of hypermetabolic feeding sites, termed syncytia, as their sole source of nutrients. The formation of the syncytium is orchestrated by the nematode in part by modulation of phytohormone responses, including cytokinin. In response to infection by the nematode H. schachtii, cytokinin signaling is transiently induced at the site of infection and in the developing syncytium. Arabidopsis lines with reduced cytokinin sensitivity show reduced susceptibility to nematode infection, indicating that cytokinin signaling is required for optimal nematode development. Furthermore, lines with increased cytokinin sensitivity also exhibit reduced nematode susceptibility. To ascertain why cytokinin hypersensitivity reduces nematode parasitism, we examined the transcriptomes in wild-type and a cytokinin-hypersensitive type-A arr Arabidopsis mutant in response to H. schachtii infection. Genes involved in the response to biotic stress and defense response were elevated in the type-A arr mutant in the absence of nematodes and were hyper-induced following H. schachtii infection, which suggests that the Arabidopsis type-A arr mutants impede nematode development because they are primed to respond to pathogen infection. These results suggest that cytokinin signaling is required for optimal H. schachtii parasitism of Arabidopsis, but that elevated cytokinin signaling triggers a heightened immune response to nematode infection.
2015-11-18 | GSE72548 | GEO
Project description:Wild type (Columbia-0) and hy5 loss of function mutants were treated with benzyl adenine (a synthetic cytokinin analog) for 1 hour and then mRNA was extracted for an RNA-seq differential expression experiment.
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Project description:GATA transcription factors are involved in multiple processes in plant growth and development. Two GATA factors, nitrate-inducible, carbon metabolism-involved (GNC) and CYTOKININ-RESPONSIVE GATA FACTOR 1 (CGA1, also named GNL) are important regulators in greening, flowering, senescence and hormone signaling. However, their direct target genes in regulating these biological processes are poorly characterized. Here, we report a genome-wide identification of the target genes of Arabidopsis GNC and CGA1.
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Project description:Wounding is a primary trigger of organ regeneration but how wound stress reactivates cell proliferation and promotes cellular reprogramming remains elusive. In this study we combined the transcriptome analysis with quantitative hormonal analysis to investigate how wounding induces callus formation in Arabidopsis thaliana. Our time-course RNA-seq analysis revealed that wounding induces dynamic transcriptional changes that can be categorized into five clusters with distinct temporal patterns. Gene ontology analyses uncovered that wounding modifies the expression of hormone biosynthesis and response genes, and quantitative analysis of endogenous plant hormones revealed accumulation of cytokinin prior to callus formation. Mutants defective in cytokinin synthesis and signalling display reduced efficiency in callus formation, indicating that de novo synthesis of cytokinin has major contribution in wound-induced callus formation. We further demonstrate that type-A ARABIDOPSIS RESPONSE REGULATOR (ARR)-mediated cytokinin signalling regulates the expression of CYCLIN D3;1 (CYCD3;1) and mutations in CYCD3;1 and its homologs CYCD3;2-3 cause defects in callus formation. Our transcriptome data, in addition, showed that wounding activates multiple developmental regulators, and we found novel roles of ETHYLENE RESPONSE FACTOR 115 (ERF115) and PLETHORA3 (PLT3), PLT5, PLT7 in wound-induced callus formation. Together, this study provides novel mechanistic insights into how wounding reactivates cell proliferation during callus formation.
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