Unknown,Transcriptomics,Genomics,Proteomics

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Chromium stress response in rice roots: effects on transcriptome proﬁles and signalling pathways responsive

ABSTRACT: Chromium (Cr) is an important environmental contaminant and also a genotoxic metal ion at high concentration, but its molecular mechanisms and signalling pathways of action in plants is still poorly unraveled. To help characterize the mechanism of molecular and signalling of rice, we present the large-scale, transcriptomic analysis of rice root responses to Cr(VI). We examined the possible involvement of reactive of reactive oxygen species (ROS) and calcium in Cr(VI) signaling transduction pathways, as well as the effect of Cr (VI) on CDPK and MAPK activity. Specially, we used the microarray assay to assess different stage Cr (VI) induced alteration in rice gene expression. This gene discovery effort will help expand our understanding of cellular responses to Cr (VI) treatment, and will identify candidate genes for enhancement of Cr resistance in crop. Two-condition experiment, short exposures and long exposures. Comparison of mock control and rice seedlings treated with 50 μM Cr(VI) during short (pooled from 1- and 3-h treatments), as compared to long (24 h) exposures.; Biological replicates: 3 control replicates (short and long exposures), 3 Cr(VI)-treated replicates (short and long exposures).

ORGANISM(S): Oryza sativa

SUBMITTER: Tsai-Lien Huang

PROVIDER: E-GEOD-41733 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Although the consequences of genotoxic injury include cell cycle arrest and apoptosis, cell survival responses after genotoxic injury can produce intrinsic death-resistance and contribute to the development of a transformed phenotype. Protein tyrosine phosphatases (PTPs) are integral components of key survival pathways, and are responsible for their inactivation, while PTP inhibition is are often associated with enhanced cell proliferation. Our aim was to elucidate signaling events that modulate cell survival after genotoxin exposure. Diploid human lung fibroblasts (HLF) were treated with Cr(VI) (as Na2CrO4), a well known human respiratory carcinogen that induces a wide spectrum of DNA damage, in the presence and absence of a broad-range PTP inhibitor, sodium orthovanadate. Notably, PTP inhibition abrogated Cr(VI)-induced clonogenic lethality. The enhanced survival of Cr(VI)-exposed cells after PTP inhibition was predominantly due to a bypass of cell cycle arrest and was not due to decreased Cr uptake as evidenced by unchanged Cr-DNA adduct burden. Additionally, the bypass of Cr-induced growth arrest by PTP inhibition, was accompanied by a decrease in Cr(VI)-induced expression of cell cycle inhibiting genes, and an increase in the Cr(VI)-induced expression of cell cycle promoting genes. Importantly, PTP inhibition resulted in an increase in forward mutations at the HPRT locus, supporting the hypothesis that PTP inhibition in the presence of DNA damage may lead to genomic instability, via bypass of cell cycle checkpoints. Experiment Overall Design: Experimental factor was chemical treatment type (3 of them) Experiment Overall Design: (1) No: HLF 1-1, HLF 1-2, HLF 1-3, HLF 1-4 Experiment Overall Design: (2) 1uM Cr(VI): HLF 3-1, HLF 3-2, HLF 3-3, HLF 3-4 Experiment Overall Design: (3) 10uM SOV + 1uM Cr(VI): HLF 4-1, HLF 4-2, HLF 4-3, HLF 4-4 Experiment Overall Design: Biological replicates: 4 different RNA extractions from 4 different cell cultures=quadruplicate per chemical treatment type

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Chromium stress response in rice roots: effects on transcriptome proﬁles and signalling pathways responsive

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