ABSTRACT: EMG produced TPA metagenomics assembly of PRJNA777294 data set (Tracking Genomic Characteristics across Oceanic Provinces: Contrasting Early and Mature Plastic Biofilm Communities).
Project description:Optimisation of DNA-protein co-extraction from the thin microbial biofilm inhabiting marine plastic debris for meta-omics and comparative metaproteomics analysis.
Project description:ovariectomized mice treated with E2+Progesterone, E2+Progesterone+TPA, E2+Progesterone+RU486 and sham for 14 days, followed by isolation of luminal mature, luminal progenitor and mammary stem cells through FACS and RNASeq performed for each cell lineage population. TPA and RU486 treated mice show significant decline in mammary stem cell pool pulation comapared to EP treated mice
Project description:Salmonella spp. biofilms have been implicated in persistence in the environment and plant surfaces. In addition, Salmonella is able to form biofilms on the surface on cholesterol gallstones. The ability of Salmonella spp. on these surfaces is superior to biofilm formation on surfaces on glass or plastic. Thus, we hypothesized that Salmonella gene expression is specific during biofilm development on cholesterol surfaces.
Project description:The basic two-step terminal differentiation model of the medullary thymic epithelial cell (mTEC) lineage from immature MHCIIlo to mature MHCIIhi mTECs has recently been extended to include a third stage namely the post-Aire MHCIIlo subset as identified by lineage-tracing models. Yet, a suitable surface marker distinguishing the phenotypically overlapping pre- from the post-Aire immature MHCIIlo stage has been lacking. Here, we introduce the lectin Tetragonolobus purpureas agglutinin (TPA) as a novel cell surface marker that allows for such delineation. Based on our data, we derived the following sequence of mTEC differentiation: TPA- MHCIIlo → TPA- MHCIIhi → TPA+ MHCIIhi → TPA+ MHCIIlo. Surprisingly, in the steady-state postnatal thymus most immature TPA- pre-Aire rather than terminally differentiated post-Aire TPA+ MHCIIlo mTECs were marked for apoptosis at an exceptionally high rate of about 70 %. Hence, only the minor cycling fraction of the MHCIIlo subset (< 20 %) potentially qualified as mTEC precursors. FoxN1 expression inversely correlated with the fraction of slow cycling and apoptotic cells within the four TPA subsets. TPA further sub-divided human mTECs, though with different subset distribution. Our revised roadmap emphazises close parallels of terminal mTEC development with that of skin, undergoing an alternative route of cell death namely cornification rather than apoptosis. The high rate of apoptosis in immature pre-Aire mTECs points to a “quality control” step during early mTEC differentiation.
Project description:The authors of this manuscript suggest the stoichiometry of outer submodules of the budding yeast kinetochore is strongly influenced by factors at the kinetochore-microtubule interface, including Fin1, Dam1, and microtubule tracking. Outer kinetochore stoichiometry is remarkably plastic and responsive to microtubule-proximal regulation.
Project description:Starvation in diploid budding yeast cells triggers a cell-fate program culminating in meiosis and spore formation. Transcription activation of early meiotic genes (EMGs) hinges on the transcription activator Ime1, its DNA-binding partner Ume6, and GSK-3 kinase Rim11. Phosphorylation of Ume6 by Rim11 is key for EMG activation. We report that Rim11 functions as the central signal integrator for controlling Ume6 phosphorylation and EMG transcription. In nutrient-rich conditions, PKA suppresses Rim11 levels, while TORC1 retains Rim11 in the cytoplasm. Inhibiting PKA and TORC1 induces Rim11 expression and nuclear localization. Remarkably, nuclear Rim11 is required, but not sufficient, for Rim11-dependent Ume6 phosphorylation. Additionally, Ime1 is an essential anchor protein for phosphorylating Ume6. Subsequently, Ume6-Ime1 coactivator complexes form, which drive EMG transcription. Our results demonstrate how varied signalling inputs (PKA/TORC1/Ime1) converge through Rim11 to regulate EMG expression and meiosis initiation. We posit that the signalling-regulatory network elucidated here generates robustness in cell-fate control.