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| Standard Gene Set Name | DUVAL_TA_NOT-IXB_UP |
| Species | Arabidopsis thaliana |
| Brief Description | Down-regulated at least 1.5-fold at 6 h of 100 nM IXB treatment (p-value < 0.05) (Table S3 PubmedID:19198845) |
| Full Description/Abstract | The plant cell wall determines cell shape and is the main barrier against environmental challenges. Perturbations in the cellulose content of the wall lead to global modifications in cellular homeostasis, as seen in cellulose synthase mutants or after inhibiting cellulose synthesis. In particular, application of inhibitors of cellulose synthesis such as thaxtomin A (TA) and isoxaben (IXB) initiates a programmed cell death (PCD) in Arabidopsis thaliana suspension cells that is dependent on de novo gene transcription. To further understand how TA and IXB activate PCD, a whole genome microarray analysis was performed on mRNA isolated from Arabidopsis suspension cells exposed to TA and IXB. More than 75% of the genes upregulated by TA were also upregulated by IXB, including genes encoding cell wall-related and calcium-binding proteins, defence/stress-related transcription factors, signalling components and cell death-related proteins. Comparisons with published transcriptional analyses revealed that half of these genes were also induced by ozone, wounding, bacterial elicitor, Yariv reagent, chitin and H2O2. These Data indicate that both IXB and TA activate a similar gene expression profile, which includes an important subset of genes generally induced in response to various biotic and abiotic stress. However, genes typically activated during the defence response mediated by classical salicylic acid, jasmonate or ethylene signalling pathways were not upregulated in response to TA and IXB. These results suggest that inhibition of cellulose synthesis induces PCD by the activation of common stress-related pathways that would somehow bypass the classical hormone-dependent defence pathways. |
| External Pathway ID/Pubmed ID | 19198845 |
| Source | Literature |
| Contributor/Author | Liming Lai and Xijin Ge |
| Organization of contributer | South Dakota State University |
| External URL | NA |