Biology subjects

Blomberg, J.

Publications and source records attributed to Blomberg, J..

3 recordsLinked to original sources

bioRxiv2023

Pseudomonas syringae infectivity correlates to altered transcript and metabolite levels of Arabidopsis Mediator mutants

Rapid metabolic responses to pathogens are essential for plant survival and depend on numerous transcription factors. Mediator is the major transcriptional co-regulator for integration and transmission of signals from transcriptional regulators to RNA polymerase II. Using four Arabidopsis Mediator mutants, med16, med18, med25 and cdk8, we studied how differences in regulation of their transcript and metabolite levels correlate to their responses to Pseudomonas syringae infection. We found that med16 and cdk8 were susceptible, while med25 showed increased resistance. Glucosinolate, phytoalexin and carbohydrate levels were reduced already before infection in med16 and cdk8, but increased in med25, which also displayed increased benzenoids levels. Early after infection, wild type plants showed reduced glucosinolate and nucleoside levels, but increases in amino acids, benzenoids, oxylipins and the phytoalexin Camalexin. The Mediator mutants showed altered levels of these metabolites and in regulation of genes encoding key enzymes for their metabolism. At later stage, mutants displayed defective levels of specific amino acids, carbohydrates, lipids and jasmonates which correlated to their infection response phenotypes. Our results reveal that MED16, MED25 and CDK8 are required for a proper, coordinated transcriptional response of genes which encode enzymes involved in important metabolic pathways for Arabidopsis responses to Pseudomonas syringae infections. HIGHLIGHTPlants need to defend themselves against different types of infections. We show that subunits of the Mediator transcriptional coactivator coordinate metabolic responses of Arabidopsis thaliana to infections by Pseudomonas syringae.

plant biology↗

bioRxiv2023

Sexual Dimorphic Gene Expression Profile of Perirenal Adipose Tissue in Ovine Fetuses with Growth Restriction.

Worldwide, fetal growth restriction (FGR) affects 7 to 10% of pregnancies, or roughly 20.5 million infants, each year. FGR not only increases neonatal mortality and morbidity but also the risk of obesity in later life. Currently, the molecular mechanisms by which FGR "programs" an obese phenotype are not well understood. Studies demonstrate that FGR females are more prone to obesity compared to males; however, the molecular mechanisms that lead to the sexually dimorphic programming of FGR are not known. Thus, we hypothesized that FGR leads to the sexually dimorphic programming of preadipocytes and reduces their ability to differentiate into mature adipocytes. To test the hypothesis, we utilized a maternal hyperthermia-induced placental insufficiency to restrict fetal growth in sheep. We collected perirenal adipose tissue from male and female near-term FGR and normal-weight fetal lambs (N=4 in each group, 16 total), examined the preadipocytes differentiation potential, and identified differential mRNA transcript expression in perirenal adipose tissue. Male FGR fetuses have lower cellular density compared to control male fetuses. However, no difference was observed in female FGR fetuses compared to control female fetuses. In addition, the ability of preadipocytes to differentiate into mature adipocytes with fat accumulation was impaired in male FGR fetuses, but this was not observed in female FGR fetuses. Finally, we examined the genes and pathways involved in the sexually dimorphic programming of obesity by FGR. On enrichment of differentially expressed genes in males compared to females, the Thermogenesis KEGG Pathway was downregulated, and the Metabolic and Steroid Biosynthesis KEGG pathways were upregulated. On enrichment of differentially expressed genes in male FGR compared to male control, the Steroid Biosynthesis KEGG Pathway was downregulated, and the PPAR Signaling KEGG pathway was upregulated. No pathways were altered in females in response to growth restriction in perirenal adipose tissue. Thus, the present study demonstrates a sexually dimorphic program in response to growth restriction in sheep fetal perirenal adipose tissue.

developmental biology↗

bioRxiv2022

Arabidopsis mutants representing each of the four Mediator modules reveal unique functions in the transcriptional response to salt stress

Changes in growth environment trigger stress responses in most organisms. The mechanisms mediating these responses are only partly understood and involve signaling pathways and transcription factors. Mediator is a conserved co-regulator complex required for transcriptional regulation of all eukaryotic protein-encoding genes. However, its function in abiotic stress responses is elusive. We here describe global gene expression changes triggered by salt stress in Arabidopsis. To explore the involvement of Mediator in salt stress response we characterized med9, med16, med18, and cdk8 mutants representing each of the four modules of Mediator. Our transcriptome data revealed enrichment of shared and specific cis-elements corresponding to unique transcription factors in promoters of mis-regulated genes for each mutant. We show that individual Mediator subunits interact with specific transcription factors to generate a transcriptional stress response and that the mutant phenotypes support the transcriptome data. med16 and med18, and to some extent cdk8, display defects in abscisic acid and anthocyanin metabolism and we identify signal molecules, transcription factors and target genes involved in these pathways as dysregulated in the Mediator mutants. Our results reveal how signals from different stress response pathways are dependent on and integrated by Mediator subunits to coordinate a functional response to salt stress.

genomics↗