Project description:In embryos, DCC binding across the length of the ~17.7 Mb X chromosome initiates at a set of recruitment elements on the X (rex). Individual rex sites collectively contribute to recruitment and repression, thus deletion of one or few rex sites causes subtle changes, as measured by mRNA-seq in mixed-stage embryos. We previously constructed a strain deleting rex-1, located ~6 kb downstream of dpy-23 (https://doi.org/10.7554/eLife.23645). Here we performed mRNA-seq in rex-1 deletion embryos.
Project description:ChIP-seq for the SDC-3 subunit of the dosage compensation complex in wild-type N2 C. elegans and Hi-C in C' elegans strains with deleted rex and extra rex sites
Project description:The transcription level of a rex-deficient S. aureus mutant in comparison to its parental strain S. aureus SH1000 was analyzed using DNA microarrays.
Project description:The objective of this comparison was to identify the impact of rex deletion on the transcriptome of Streptococcus pneumoniae D39. This comparison showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. In this study, we investigated the transcriptomic response of Streptococcus pneumoniae D39 to NADH. Transcriptome comparison of the D39 wild-type grown in chemically-defined medium (CDM) with 0 mg/ml NADH to 0.5 mg/ml NADH revealed elevated expression of various genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in the transport and biosynthesis of niacin. Microarray results were further confirmed by β-galactosidase assays. Promoter-lacZ fusions assays and microarray studies showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. The putative operator site of Rex in the promoter regions of Rex-regulated genes is predicted and confirmed by promoter mutational experiments.
