Effect of biotin deficiency on gene expression in Aravbidopsis leaves
Ontology highlight
ABSTRACT: In addition to its essential metabolic functions biotin is suggested a critical role in regulating gene expression. The first committed enzyme in biotin biosynthesis in Arabidopsis, 7-keto-8-aminopelargonic acid synthase is encoded by At5g04620 (BIO4). We isolated a novel T-DNA insertion mutant of BIO4 (bio4-1) showing a spontaneous cell death phenotype that could be rescued both by exogenous biotin and genetic complementation. The bio4-1 plants exhibited massive accumulation of hydrogen peroxide. The T-DNA insertion in the bio4-1 mutant contains a Methionine Sulfoxide Reductase B9 (AT4G21850) under a constitutive 35S CaMV promoter. To dissect the specific effects of biotin defiency on gene expression on a genome wide scale, we compared expression of wt Col-0 leaves with bio4-1 mutants and bio4-1 mutants complemented with D-biotin.
Project description:In addition to its essential metabolic functions biotin is suggested a critical role in regulating gene expression. The first committed enzyme in biotin biosynthesis in Arabidopsis, 7-keto-8-aminopelargonic acid synthase is encoded by At5g04620 (BIO4). We isolated a novel T-DNA insertion mutant of BIO4 (bio4-1) showing a spontaneous cell death phenotype that could be rescued both by exogenous biotin and genetic complementation. The bio4-1 plants exhibited massive accumulation of hydrogen peroxide. The T-DNA insertion in the bio4-1 mutant contains a Methionine Sulfoxide Reductase B9 (AT4G21850) under a constitutive 35S CaMV promoter. To dissect the specific effects of biotin defiency on gene expression on a genome wide scale, we compared expression of wt Col-0 leaves with bio4-1 mutants and bio4-1 mutants complemented with D-biotin. Expression in leaves of Col-0 wt, bio4-1 mutants with a T-DNA insertion in the 5`-UTR of BIO4, and bio4-1 mutants complemented with watering with 200µM D-biotin.
Project description:The purpose of the study is to assess a new treatment for patients with liver tumor metastases from colorectal cancer. The treatment has never been used in humans before. The treatment foresees the use of two compounds: AvdinOX and [177Lu]DOTA-biotin.
AvidinOX is a new compound, essentially a natural protein obtained from hen eggs, while [177Lu]DOTA-biotin is a new chemical compound resulting from the combination of the DOTA-biotin (also deriving from a natural vitamin which is biotin) with the 177Lutetium, an atom which emits radiation.
AvidinOX will be injected directly into the metastases in the liver and [177Lu]DOTA-biotin will be injected into the arm vein.
One specific property of AvidinOX is that it chemically links to the tumor tissues when it is injected while maintaining the capacity to take up [177Lu]DOTA-biotin. Once locally bound in tumor tissue, AvidinOX becomes an "artificial receptor" for intravenously injected [177Lu]DOTA-biotin, which allows an internal radiation therapy of the tumor tissue.
The treatment of liver metastases with local injection of AvidinOX and the following intra-venous injection of [177Lu]DOTA-biotin could be simpler and more tolerable than the current available treatments.
Project description:To further understand how RVE5 controls thermo-responses, we generated RVE5-MYC overexpression plants with the CaMV 35S promoter. Using these RVE5-MYC overexpression plants grown at 29°C, we performed Chromatin Immunoprecipitation-Sequencing (ChIP-Seq).
Project description:Mutations in MECP2 cause Rett syndrome (RTT), a X-linked neurological disorder characterized by the regressive loss of neurodevelopmental milestones and acquired intellectual disability and motor impairments. However, the cellular heterogeneity of the mammalian brain impedes our understanding of how MECP2 mutations disrupt neuronal function and contribute to RTT. In response, we developed cell type-specific biotin tagging in mice bearing RTT-associated mutations and profiled nuclear transcriptomes in WT and mutant neurons. Although individual gene expression changes are largely specific to each mutation and cell type, higher-level transcriptional features remain conserved and correlate with RTT phenotypic severity. Furthermore, subcellular RNA populations support post-transcriptional compensation as a basis for the upregulation of long genes previously reported in RTT mutant neurons. Finally, we overcame the genetic mosacism associated with female RTT mouse models and identified functionally distinct gene expression changes in neighboring WT and mutant neurons, which altogether provide key contextual insights into RTT.
Project description:Arabidopsis emf2 mutants bypass vegetative development and flowering upon seed germination. We introduced a broccoli BoEMF2.1 gene into emf2 mutants and obtained rescued emf2 plants that harbored 35S::BoEMF2.1. We found that BoEMF2.1 can partially rescue the phenotype of emf2 to that of WT. We used microarrays to study the global program of gene expression and to identify genes misexpressed in the Arabidopsis emf2 mutant that had been rescued by 35S::BoEMF2.1.