Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.
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ABSTRACT:
PROVIDER: PRJNA1302476 | ENA |
REPOSITORIES: ENA
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Project description:The microarrays experiments was performed in order to identify transcriptional networks in Enterococcus faecalis. Work:Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure
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Project description:Mitochondrial dynamics are central to maintaining liver metabolic homeostasis, yet the mechanisms that safeguard mitochondrial integrity during development and metabolic dysfunction remain poorly defined. Here, we identify Family with sequence similarity 210 member A (FAM210A) as a hepatocyte-enriched mitochondrial regulator essential for postnatal liver maturation. Hepatocyte-specific deletion of Fam210a (Fam210aHKO) in mice caused early growth restriction, reduced body and liver mass, and pronounced hepatic steatosis with glycogen depletion. These defects were accompanied by lower postprandial glucose levels in the fastedre–feeding state, impaired oxidative phosphorylation, reduced mtDNA content, and abnormal cristae architecture. Transcriptomic and proteomic profiling revealed broad suppression of fatty acid, sterol, and bile acid metabolism, with concomitant glutathione stress responses. Mechanistically, FAM210A deficiency induces excessive OPA1 cleavage and cristae destabilization, potentially by disrupting YME1L function. Strikingly, these juvenile defects were transient and resolved by adulthood, underpinned by enhanced hepatocyte proliferation and mitochondrial biogenesis, consistent with a compensatory stress-adaptive response via the activation of ISR signaling. Together, these findings uncover FAM210A as a developmental safeguard of mitochondrial remodeling in hepatocytes and indicate compensatory programs with therapeutic relevance for chronic liver disease.
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Project description:High-risk B-cell acute lymphoblastic leukemia (B-ALL) remains a therapeutic challenge despite advances in the use of tyrosine kinase inhibitors and chimeric- antigen-receptor engineered T cells. Lymphoblastic-leukemia precursors are highly sensitive to oxidative stress. KLF5 is a member of the Krüppel-like family of transcription factors. KLF5 expression is repressed in B-ALL, including BCR-ABL1+ B-ALL. Here, we demonstrate that forced expression of KLF5 in B-ALL cells bypasses imatinib resistance not associated with mutations of BCR-ABL. Expression of Klf5 impaired leukemogenic activity of BCR-ABL1+ B-cell precursors in vitro and in vivo. The complete genetic loss of Klf5 reduced oxidative stress, increased regeneration of reduced glutathione and decreased apoptosis of leukemic precursors. Klf5 regulation of glutathione levels was mediated by its regulation of glutathione-S-transferase Mu 1 (Gstm1), an important regulator of glutathione-mediated detoxification and protein glutathionylation. Expression of Klf5 or the direct Klf5 target gene Gstm1 inhibited clonogenic activity of Klf5∆/∆ leukemic B-cell precursors and unveiled a Klf5-dependent regulatory loop on glutamine-dependent glutathione metabolism. In summary, we describe a novel mechanism of Klf5 B-ALL suppressor activity through its direct role on the metabolism of antioxidant glutathione levels, a crucial positive regulator of leukemic precursor survival.
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Project description:rs08-03_glutathion - glutathion - How does glutathione content or reduction state affect H2O2-induced changes in the transcriptome? - Three single Arabidopsis mutants were used: cat2, knockout for catalase2 and so enriched in H2O2; cad2, defective in glutathione content; cytGR, knockout for cytosolic glutathione reductase. Cat2 was crossed with cad2 and cyt GR, and col0, 3 single mutants, and 2 double mutants were sampled in controlled growth conditions either in 8h or 16h photoperiod. Keywords: gene knock out 20 dye-swap pairs - CATMA arrays: 40 arrays
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Project description:Plant compensatory responses depends on transcriptional reprogramming. We used microarray analysis to understand the differential gene expression pattern between clipped (herbivore browsed) and unclipped plant. Arabidopsis ecotypes Columbia and Landsberg erecta were chosen due to their differential compensatory response. The plants were grown in greenhouse. At bolting stage the plants were clipped to imitate herbivore damage. Following day the samples were collected from clipped and unclipped plants.
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