ABSTRACT: Identifying large-scale recombination and capsular switching events in Streptococcus agalactiae strains causing disease in adults in the United Kingdom between 2014 and 2015
Project description:The lysine 23 of histone H3 (H3K23me2) positively correlates with H3K9me3 and H3K27me3, marks enriched in heterochromatic regions (Ho, J.W. et al., 2014; Garrigues, J.M. et al., 2015; Liu, T. et al., 2015), and negatively correlates with H3K36me2/3 and H3K23/27ac, modifications enriched in actively transcribed regions. Similarly to the reported distribution of H3K9me3 (Ho, J.W. et al., 2014; Garrigues, J.M. et al., 2015), H3K23me2 is enriched on autosomal arms and is depleted from the central regions of the autosomes and from most of the lenght of the X chromosome.
Project description:Purpose: We recently reported that isogenic deletion of lysine decarboxylase (ΔcadA/SP_0916), an enzyme that catalyzes the biosynthesis of polyamine cadaverine in Streptococcus pneumoniae TIGR4 results in loss of capsular polysaccharide (CPS), which constitutes a novel mechanism of regulation of CPS. Here, we conducted RNA-Seq to elucidate molecular mechanisms of CPS regulation in polyamine synthesis impaired pneumococci. Result: Significantly differentially expressed genes in ΔcadA represent pneumococcal pathways involved in the biosynthesis of precursors for CPS and peptidoglycan. Conclusion: We establish a possible link and interchange between two cellular processes such as high energy demanding capsule production and oxidative stress responses in polyamine synthesis impaired pneumococci (ΔcadA).
Project description:Lewy body (LB) pathology and loss of dopaminergic neurons are imprints of Parkinson’s disease (PD). LBs are mainly comprised of alpha-Synuclein (Dijkstra et al., 2014). Strolling detection of LBs in brain regions contribute to progressive construct of PD pathology to which molecular mechanisms are not clear (H. Braak & Del Tredici, 2017). Two key facets of LB formation are protein aggregation via misfolding and transmission of misfoldled proteins to various brain regions, eventually causing neuronal death (Goedert, Spillantini, Del Tredici, & Braak, 2013; Pacelli et al., 2015). Misfolding requires alterations in intracellular physiology (Carbone, Costa, Provensi, Mannaioni, & Masi, 2017; Funes et al., 2014; Guzman et al., 2018; Pacelli et al., 2015) and detection of misfolded proteins in exosomes confirms exosomatic transmission (Ngolab et al., 2017). High levels of neurotropic-factors (Brockmann et al., 2017) and changes in bioenergetics are found in PD patients, these can bring physiological alterations (Smith et al., 2018). En masse, these evidences and hipocampal association with synucleopathies (Flores-Cuadrado, Ubeda-Bañon, Saiz-Sanchez, de la Rosa-Prieto, & Martinez-Marcos, 2016) allowed us to probe other volunerable PD proteins in cell-lysate and exosomal proteomes of bFGF treated hippocampal neurons. Using WPCNA we developed co-expression modules and spotted many PD related proteins; which can act as precursors during diseased or onset stage.
Project description:7 days old protonema of Physcomitrella patens Wildtype and two transgenic lines, ΔPpcmt line 281 (Noy-Malka et al. 2014; IMSC accession 40738) and ΔPpmet line 5 (Yaari et al. 2015; IMSC accession 40758) grown on BCDAT solid medium.
