Project description:Salivary gland-specific binding assays reveal that CrebA, a bZIP transcription factor, directly binds the vast majority of genes encoding the secretory machinery, including proteins of the signal recognition particle and receptor, proteins involved in co-translational import of cargo into the ER, proteins involved in vesicular transport between the ER and Golgi, as well as the structural proteins and enzymes of these organelles. CrebA does not bind salivary gland-specific cargo genes. Instead, it binds and boosts expression of Sage, which encodes a bHLH transcription factor that upregulates cargo expression. CrebA also directly binds and upregulates Xbp1, which encodes a key factor in the unfolded protein response, and Tudor-SN, which encodes a protein that in other systems increases secretory cargo mRNA levels.
Project description:To reveal novel molecular factors behind the development of salivary gland cancer, we performed gene expression analyses from Smgb-Tag mouse salivary gland samples. The overall purpose was to apply these results for clinical use to find new approaches for both possible therapeutic targets and more accurate diagnostic tools in identification of salivary gland cancers. Smgb-Tag mouse strain, in which salivary neoplasms arise through a dysplastic phase in submandibular glands, was investigated using genome-wide microarray expression analysis, Ingenuity pathway analysis, RT-PCR, and immunohistochemistry.
Project description:To reveal novel molecular factors behind the development of salivary gland cancer, we performed gene expression analyses from Smgb-Tag mouse salivary gland samples. The overall purpose was to apply these results for clinical use to find new approaches for both possible therapeutic targets and more accurate diagnostic tools in identification of salivary gland cancers. Smgb-Tag mouse strain, in which salivary neoplasms arise through a dysplastic phase in submandibular glands, was investigated using genome-wide microarray expression analysis, Ingenuity pathway analysis, RT-PCR, and immunohistochemistry. 3 normal, 3 dysplastic, and 3 adenocarcinomatous submandibular gland tumours of Smgb-Tag mice.
Project description:As we observed that salivary gland ablation induced retardation of systemic growth, it raised the possibility that salivary glands might secrete a growth factor-like peptide into the hemolymph to regulate systemic growth. To identify potential salivary gland-derived peptides with endocrine activity, we performed liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis and investigated the changes in the hemolymph proteome following salivary gland ablation.
Project description:We use mRNA-seq to transcriptionally profile larval salivary gland tissue from Drosophila third instar larvae. These data provide insights into tissue physiology and can be used to identify tissue specific transcripts.
Project description:modENCODE_submission_722 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Most terminally differentiated Drosophila tissues are either polyploid or polytene. Unlike normal chromosomes, where the entire chromosome must be replicated exactly once, polytene chromosomes are often differentially replicated with many regions underreplicated and some overreplicated. We will characterize five different polytene tissues using comparative genomic hybridization (CGH) to identify differentially replicated regions of each chromosome. These studies will also identify tissue specific amplicons, where the replication mediated amplification of specific loci is essential for up-regulation of mRNA levels encoding proteins critical for development. The differential replication of polytene chromosomes in Drosophila will provide a unique opportunity to understand how developmental cues and chromosomal domains influence replication initiation. Keywords: CGH For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CGH. BIOLOGICAL SOURCE 1: Strain: Oregon-R Orr-Weaver; Developmental Stage: Embryo 0-4h; Genotype: TBA; Sex: Unknown; BIOLOGICAL SOURCE 2: Strain: Oregon-R Orr-Weaver; Tissue: larval salivary gland; Genotype: TBA; Sex: Unknown; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: Tissue larval salivary gland
Project description:Salivary glands that produce and secret saliva, which is essential for lubrication, digestion, immunity, and oral homeostasis, consist of diverse cells. The long-term maintenance of diverse salivary gland cells in organoids remains problematic. Here, we established long-term murine salivary gland organoids from 3 major salivary glands, including parotid gland (PG), submandibular gland (SMG), and sublingual gland (SLG). Murine salivary gland organoids expressed gland-specific genes and proteins of acinar, myoepithelial, and duct cells. Organoids were maintained in growth media (named GEM) and further underwent differentiation in differentiation media (named DAM). Our study will provide an experimental platform for the exploration of mechanisms involvled in tissue regeneration, development, or several salivary gland diseases.
Project description:We replaced the endogenous histones of Drosophila melanogaster with either histones containing an H3K9R mutation or histones containing an H4K16R mutation to interrogate direct functions for histone residues in salivary gland endoreplication. We performed genomic DNA sequencing in HWT (Histone Wild Type) control, H3K9R, and H4K16R females. We found that H3K9 promotes under-replication of pericentromeric heterochromatin but not along chromosome arms and H4K16 is dispensable for under-replication.
Project description:Loss of Irf6 leads to disruption of branching morphogenesis and secretory acnii formation in salivary gland. To determine the differentially expressed genes in Irf6 mutant, embryonic salivary gland tissues were extracted at E14.5.
Project description:Salivary gland hypofunction is a common adverse effect during and after radiotherapy of head and neck cancers, resulting in the dry mouth syndrome called xerostomia. Previous studies suggested that the functionality of the salivary gland is under the regulation of the circadian clock, however, the extent and scope of this regulation remains unexplored. Here, we profiled the diurnal fluctuation of gene expression in the mouse submandibular salivary gland. We further analyzed the regulatory role of key circadian transcription factors Bmal1, Nr1d1 (Rev-erba), and Dbp, which revealed a wide range of potential down-stream target genes. The circadian clock was disrupted upon irradiation, as revealed by gene expression analysis. We propose that the mechanism of salivary gland hypofunction in radiotherapy involves perturbation of the circadian clock.