Project description:Investigation of whole genome gene expression level changes in Lactococcus lactis KCTC 3769T,L. raffinolactis DSM 20443T, L. plantarum DSM 20686T, L. fujiensis JSM 16395T, L. garvieae KCTC 3772T, L. piscium DSM 6634T and L. chungangensis CAU 28T . This proves that transcriptional profiling can facilitate in elucidating the genetic distance between closely related strains.
Project description:Investigation of whole genome gene expression level changes in Lactococcus lactis KCTC 3769T,L. raffinolactis DSM 20443T, L. plantarum DSM 20686T, L. fujiensis JSM 16395T, L. garvieae KCTC 3772T, L. piscium DSM 6634T and L. chungangensis CAU 28T . This proves that transcriptional profiling can facilitate in elucidating the genetic distance between closely related strains. A one chip study using total RNA recovered from of L. raffinolactis DSM 20443T, L. plantarum DSM 20686T, L. fujiensis JSM 16395T, L. garvieae KCTC 3772T, L. piscium DSM 6634T and L. chungangensis CAU 28T . For the the transcriptome of of L. raffinolactis DSM 20443T, L. plantarum DSM 20686T, L. fujiensis JSM 16395T, L. garvieae KCTC 3772T, L. piscium DSM 6634T and L. chungangensis CAU 28T was analyzed using the Lactococcus lactis KCTC 3769T microarray platform
Project description:The expression profile of C. autoethanogenum DSM 10061 grown autotrophically with H2:CO:CO2 under visible light at an intensity of 4200 lux versus the expression profile of C. autoethanogenum DSM 10061 grown autotrophically in the dark
Project description:Aberrant alternative splicing of mRNAs results in dysregulated gene expression in multiple neurological disorders. Here we show that hundreds of mRNAs are incorrectly expressed and spliced in white blood cells and brain tissue of individuals with fragile X syndrome (FXS). Surprisingly, the FMR1 (Fragile X Messenger Ribonucleoprotein 1) gene is transcribed in >70% of the FXS tissues. In all FMR1 expressing FXS tissues, FMR1 RNA itself is mis-spliced in a CGG expansion-dependent manner to generate the little-known FMR1-217 RNA isoform, which is comprised of FMR1 exon 1 and a pseudo-exon in intron 1. FMR1-217 is also expressed in FXS premutation carrier-derived skin fibroblasts and brain tissue. We show that in cells aberrantly expressing mis-spliced FMR1, antisense oligonucleotide (ASO) treatment reduces FMR1-217, rescues full-length FMR1 RNA, and restores FMRP (Fragile X Messenger RibonucleoProtein) to normal levels. Notably, FMR1 gene reactivation in transcriptionally silent FXS cells using 5-aza-2′-deoxycytidine (5-AzadC), which prevents DNA methylation, increases FMR1-217 RNA levels but not FMRP. ASO treatment of cells prior to 5-AzadC application rescues full-length FMR1 expression and restores FMRP. These findings indicate that mis-regulated RNA processing events in blood could serve as potent biomarkers for FXS and that in those individuals expressing FMR1-217, ASO treatment may offer a new therapeutic approach to mitigate the disorder.