Transgenerational effects of chromium stress at phenotypic and molecular level in Arabidopsis thaliana
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Arabidopsis thaliana
SUBMITTER: Matteo Buti
PROVIDER: E-MTAB-11099 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Soil salinity is a major environmental stress that restricts crop growth and yield. Here, crucial proteins and biological pathways were investigated under salt-stress and recovery conditions in Tritipyrum “Y1805” to explore its salt-tolerance mechanism. In total, 44 and 102 differentially expressed proteins (DEPs) were identified in “Y1805” under salt-stress and recovery conditions, respectively. A proteome-transcriptome-associated analysis revealed that the expression patterns of 13 and 25 DEPs were the same under salt-stress and recovery conditions, respectively. “Response to stimulus”, “antioxidant activity”, “carbohydrate metabolism”, “amino acid metabolism”, “signal transduction”, “transport and catabolism” and “biosynthesis of other secondary metabolites” were present under both conditions in “Y1805”. In addition, “energy metabolism” and “lipid metabolism” were recovery-specific pathways, while “antioxidant activity”, and “molecular function regulator” under salt-stress conditions, and “virion” and “virion part” during recovery, were “Y1805”-specific compared with the salt-sensitive wheat “Chinese Spring”. “Y1805” contained 83 specific DEPs related to salt-stress responses. The strong salt tolerance of “Y1805” could be attributed to the strengthened cell walls, reactive oxygen species scavenging, osmoregulation, phytohormone regulation, transient growth arrest, enhanced respiration, ammonium detoxification, transcriptional regulation and error information processing. These data will facilitate an understanding of the molecular mechanisms of salt tolerance and aid in the breeding of salt-tolerant wheat.
2021-12-08 | PXD026671 | Pride
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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