Data Catalog

Multiple cell types can be specified from a single pool of progenitors through the combinatorial activity of transcriptional regulators, which activate distinct developmental programs to establish different cell fates. The zinc finger transcription factor Glass is required for neuronal progenitors in the Drosophila eye imaginal disc to acquire a photoreceptor identity. Glass is also expressed in non-neuronal cone and pigment cells, but its role in these cells is unknown. To examine how Glass activity is affected by the cellular context, the researchers misexpressed it in different tissues. When expressed in neuroblasts of the larval brain or in epithelial cells of the wing disc, Glass activated both a common core set of target genes and distinct gene sets specific to each tissue. In addition to photoreceptor-specific genes, Glass induced markers of cone and pigment cells. Cell type-specific glass mutations generated in cone or pigment cells using somatic CRISPR revealed autonomous developmental defects, and expressing Glass specifically in these cells partially rescued glass mutant phenotypes. Glass thus acts in both neuronal and non-neuronal cells to promote their differentiation into functional components of the eye, suggesting that it is a determinant of organ identity.

Glial cells play structural and functional roles central to the formation, activity and integrity of neurons throughout the nervous system. Here, using the genetic model Drosophila melanogaster, reseearchers identify a new glial cell type in one of the most active tissues in the nervous system—the retina. These cells, called ommatidial cone cells (or Semper cells), were previously recognized for their role in lens formation. Using cell-specific molecular genetic approaches, this study demonstrates that cone cells (CCs) also share molecular, functional, and genetic features with both vertebrate and invertebrate glia to prevent light-induced retinal degeneration and provide structural and physiological support for photoreceptors.

Trophoblast stem (TS) cells derived from the trophectoderm (TE) of mammalian embryos have the ability to self-renew indefinitely or differentiate into fetal lineages of the placenta. Epigenetic control of gene expression plays an instrumental role in dictating the fate of TS cell self-renewal and differentiation. However, the roles of histone demethylases and activating histone modifications such as methylation of histone 3 lysine 4 (H3K4me3/me2) in regulating TS cell expression programs, and in priming the epigenetic landscape for trophoblast differentiation, are largely unknown. This study demonstrates that the H3K4 demethylase, KDM5B, regulates the H3K4 methylome and expression landscapes of TS cells. Depletion of KDM5B resulted in downregulation of TS cell self-renewal genes and upregulation of trophoblast-lineage genes, which was accompanied by altered H3K4 methylation. Moreover, it is found that KDM5B resets the H3K4 methylation landscape during differentiation in the absence of the external self-renewal signal, FGF4, by removing H3K4 methylation from promoters of self-renewal genes, and of genes whose expression is enriched in TS cells. Altogether, these data indicate an epigenetic role for KDM5B in regulating H3K4 methylation in TS cells and during trophoblast differentiation.

Positioning of nucleosomes along DNA is an integral regulator of chromatin accessibility and gene expression in diverse cell types. However, the precise nature of how histone demethylases including the histone 3 lysine 4 (H3K4) demethylase, KDM5B, impacts nucleosome positioning around transcriptional start sites (TSS) of active genes is poorly understood. Therefore, to clarify the role for KDM5B in regulating nucleosome organization in ES cells, this study evaluated genome-wide changes in nucleosome positioning in KDM5B-depleted and control ES cells using micrococcal nuclease sequencing (MNase-Seq). These findings demonstrate that depletion of KDM5B leads to altered enrichment of nucleosomes around TSS regions and accessible chromatin regions (DNase I hypersensitive sites).

Phosophoproteomic analysis was used to profile cell lines in the MCF-10A lineage of human mammary epithelial cells to determine how human breast cells can be reprogrammed during tumorigenic progression. Data were collected using a LTQ-XL mass spectrometer (Thermo). Phosphopeptides were enriched from cell extracts from 3 independent biological replicates, and each replicate was analyzed as 3 technical replicates for a total of 9 LC/MS/MS runs per cell line.

B-cells play a pivotal role in several autoimmune diseases, including patients with immune-mediated neurological disorders (PIMND), such as neuromyelitis optica (NMO), multiple sclerosis (MS), and myasthenia gravis (MG). Targeting B-cells has been an effective approach in ameliorating both central and peripheral autoimmune diseases. However, there is a paucity of literature on the safety of continuous B-cell depletion over a long period of time. The aim of this study was to examine the long-term safety, incidence of infections, and malignancies in subjects receiving continuous therapy with a B-cell depleting agent rituximab over at least 3 years or longer. This was a retrospective study involving PIMND who received continuous cycles of rituximab infusions every 6 to 9 months for up to 7 years. The incidence of infection related adverse events (AE), serious adverse events (SAE), and malignancies were observed.

Proteomics data from a study on whether mercury exposure alters B cell responsiveness to self-antigens by interfering with B cell receptor (BCR) signal transduction. These data show the effects of mercury on the protein tyrosine kinase SYK, a critical protein involved in regulation of the BCR signaling pathway. The raw data for quantitation of SYK phosphorylation status of selected sites were obtained using multiple reaction monitoring (MRM) on a TSQ triple quadrupole mass spectrometer.

Müller glia in the zebrafish retina respond to retinal damage by re-entering the cell cycle, which generates large numbers of retinal progenitors that ultimately replace the lost neurons. In this study, researchers compared the regenerative outcomes of adult zebrafish exposed to one round of phototoxic treatment with adult zebrafish exposed to six consecutive rounds of phototoxic treatment. It was observed that Müller glia continued to re-enter the cell cycle to produce clusters of retinal progenitors in zebrafish exposed to multiple rounds of phototoxic light.