Expression patterns of Wnts, Frizzleds, sFRPs, and misexpression in transgenic mice suggesting a role for Wnts in pancreas and foregut pattern formation

2002 ◽  
Vol 225 (3) ◽  
pp. 260-270 ◽  
Author(s):  
R. Scott Heller ◽  
Darwin S. Dichmann ◽  
Jan Jensen ◽  
Chris Miller ◽  
Gordon Wong ◽  
...  
Keyword(s):  
Pattern Formation ◽  
Transgenic Mice ◽  
Expression Patterns

scholarly journals Transgene expression of steel factor in the basal layer of epidermis promotes survival, proliferation, differentiation and migration of melanocyte precursors

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2915-2923 ◽  
Author(s):  
T. Kunisada ◽  
H. Yoshida ◽  
H. Yamazaki ◽  
A. Miyamoto ◽  
H. Hemmi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Transgenic Mice ◽  
Germ Cells ◽  
Expression Patterns ◽  
Basal Layer ◽  
Epidermal Keratinocytes ◽  
Oral Epithelium ◽  
Developmental Defects ◽  
Steel Factor

Mutations at the murine dominant white spotting (KitW) and steel (MgfSl) loci, encoding c-Kit receptor kinase and its ligand respectively, exert developmental defects on hematopoietic cells, melanocytes, germ cells and interstitial cells of Cajal. The expression patterns of steel factor (SLF) observed in the skin and gonads suggest that SLF mediates a migratory or a chemotactic signal for c-Kit-expressing stem cells (melanocyte precursors and primordial germ cells). By targeting expression of SLF to epidermal keratinocytes in mice, we observed extended distribution of melanocytes in a number of sites including oral epithelium and footpads where neither melanocytes nor their precursors are normally detected. In addition, enlarged pigmented spots of KitW and other spotting mutant mice were observed in the presence of the SLF transgene. These results provide direct evidence that SLF stimulates migration of melanocytes in vivo. We also present data suggesting that SLF does not simply support survival and proliferation of melanocytes but also promotes differentiation of these cells. Unexpectedly, melanocyte stem cells independent of the c-Kit signal were maintained in the skin of the SLF transgenic mice. After the elimination of c-Kit-dependent melanoblasts by function-blocking anti-c-Kit antibody, these stem cells continued to proliferate and differentiate into mature melanocytes. These melanoblasts are able to migrate to cover most of the epidermis after several months. The SLF transgenic mice described in this report will be useful in the study of melanocyte biology.

Differential expression of the closely linked KISS1, REN, and FLJ10761 genes in transgenic mice

2004 ◽  
Vol 17 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Ravi Nistala ◽  
Xiaoji Zhang ◽  
Curt D. Sigmund
Keyword(s):  
Transgenic Mice ◽  
Human Chromosome ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Artificial Chromosome ◽  
Chromosome 1 ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression ◽  
Human Chromosome 1

We previously reported the development and characterization of transgenic mice containing a large 160-kb P1 artificial chromosome (PAC) encompassing the renin (REN) locus from human chromosome 1. Here we demonstrate that PAC160 not only encodes REN, but also complete copies of the next upstream (KISS1) and downstream ( FLJ10761 ) gene along human chromosome 1. Incomplete copies of the second upstream (PEPP3) and downstream (SOX13) genes are also present. The gene order PEPP3-KISS1-REN-FLJ10761-SOX13 is conserved in mice containing either one or two copies of the REN locus. Despite the close localization of KISS1, REN, and FLJ10761 , they each exhibit distinct, yet overlapping tissue-specific expression profiles in humans. The tissue-specific expression patterns of REN and FLJ10761 were retained in transgenic mice containing PAC160. Expression of REN and FLJ10761 were also proportional to copy number. Expression of KISS1 in PAC160 mice showed both similarities and differences to humans. These data suggest that expression of gene blocks encoded on large genomic clones are retained when the clones are used to generate transgenic mice. Genomic elements which act to insulate genes from their neighbors are also apparently retained.

scholarly journals Exploring miRNA-mRNA regulatory network in cardiac pathology in Na+/H+ exchanger isoform 1 transgenic mice

2018 ◽  
Vol 50 (10) ◽  
pp. 846-861 ◽  
Author(s):  
Jin Xue ◽  
Dan Zhou ◽  
Orit Poulsen ◽  
Iain Hartley ◽  
Toshihiro Imamura ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Transgenic Mice ◽  
Cardiac Hypertrophy ◽  
Rna Sequencing ◽  
High Throughput Sequencing ◽  
Interstitial Fibrosis ◽  
Expression Patterns ◽  
Cardiac Injury ◽  
Differentially Expressed ◽  
Mrna Targets

Numerous studies have demonstrated that Na+/H+ exchanger isoform 1 (NHE1) is elevated in myocardial diseases and its effect is detrimental. To better understand the involvement of NHE1, we have previously studied cardiac-specific NHE1 transgenic mice and shown that these mice develop cardiac hypertrophy, interstitial fibrosis, and cardiac dysfunction. The purpose of current study was to identify microRNAs and their mRNA targets involved in NHE1-mediated cardiac injury. An unbiased high-throughput sequencing study was performed on both microRNAs and mRNAs. RNA sequencing showed that differentially expressed genes were enriched in hypertrophic cardiomyopathy pathway by Kyoto Encyclopedia of Genes and Genomes annotation in NHE1 transgenic hearts. These genes were classified as contraction defects (e.g., Myl2, Myh6, Mybpc3, and Actb), impaired intracellular Ca2+ homeostasis (e.g., SERCA2a, Ryr2, Rcan1, and CaMKII delta), and signaling molecules for hypertrophic cardiomyopathy (e.g., Itga/b, IGF-1, Tgfb2/3, and Prkaa1/2). microRNA sequencing revealed that 15 microRNAs were differentially expressed (2-fold, P < 0.05). Six of them (miR-1, miR-208a-3p, miR-199a-5p, miR-21-5p, miR-146a-5p, and miR-30c-5p) were reported to be related to cardiac pathological functions. The integrative analysis of microRNA and RNA sequencing data identified several crucial microRNAs including miR-30c-5p, miR-199a-5p, miR-21-5p, and miR-34a-5p as well as 10 of their mRNA targets that may affect the heart via NFAT hypertrophy and cardiac hypertrophy signaling. Furthermore, important microRNAs and mRNA targets were validated by quantitative PCR. Our study comprehensively characterizes the expression patterns of microRNAs and mRNAs, establishes functional microRNA-mRNA pairs, elucidates the potential signaling pathways, and provides novel insights on the mechanisms underlying NHE1-medicated cardiac injury.

scholarly journals How Boundaries Form: Linked Nonautonomous Feedback Loops Regulate Pattern Formation in Yeast Colonies

Genetics ◽  
2019 ◽  
Vol 213 (4) ◽  
pp. 1373-1386
Author(s):  
Sarah Piccirillo ◽  
Abbigail H. McCune ◽  
Samuel R. Dedert ◽  
Cassandra G. Kempf ◽  
Brian Jimenez ◽  
...  
Keyword(s):  
Pattern Formation ◽  
Cell Fate ◽  
Positive Feedback ◽  
Expression Patterns ◽  
Feedback Loops ◽  
General Mechanism ◽  
Colony Development ◽  
Feeder Cells ◽  
Link Type ◽  
A Cell

Under conditions in which budding yeast form colonies and then undergo meiosis/sporulation, the resulting colonies are organized such that a sharply defined layer of meiotic cells overlays a layer of unsporulated cells termed “feeder cells.” This differentiation pattern requires activation of both the Rlm1/cell-wall integrity pathway and the Rim101/alkaline-response pathway. In the current study, we analyzed the connection between these two signaling pathways in regulating colony development by determining expression patterns and cell-autonomy relationships. We present evidence that two parallel cell-nonautonomous positive-feedback loops are active in colony patterning, an Rlm1-Slt2 loop active in feeder cells and an Rim101-Ime1 loop active in meiotic cells. The Rlm1-Slt2 loop is expressed first and subsequently activates the Rim101-Ime1 loop through a cell-nonautonomous mechanism. Once activated, each feedback loop activates the cell fate specific to its colony region. At the same time, cell-autonomous mechanisms inhibit ectopic fates within these regions. In addition, once the second loop is active, it represses the first loop through a cell-nonautonomous mechanism. Linked cell-nonautonomous positive-feedback loops, by amplifying small differences in microenvironments, may be a general mechanism for pattern formation in yeast and other organisms.

scholarly journals IL-15 Overexpression Promotes Endurance, Oxidative Energy Metabolism, and Muscle PPARδ, SIRT1, PGC-1α, and PGC-1β Expression in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 232-245 ◽  
Author(s):  
LeBris S. Quinn ◽  
Barbara G. Anderson ◽  
Jennifer D. Conner ◽  
Tami Wolden-Hanson
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Transgenic Mice ◽  
Oxidative Metabolism ◽  
Troponin I ◽  
Expression Patterns ◽  
Sirtuin 1 ◽  
Ppar Γ ◽  
Oxidative Energy Metabolism

Endurance exercise initiates a pattern of gene expression that promotes fat oxidation, which in turn improves endurance, body composition, and insulin sensitivity. The signals from exercise that initiate these pathways have not been completely characterized. IL-15 is a cytokine that is up-regulated in skeletal muscle after exercise and correlates with leanness and insulin sensitivity. To determine whether IL-15 can induce any of the metabolic adaptations associated with exercise, substrate metabolism, endurance, and molecular expression patterns were examined in male transgenic mice with constitutively elevated muscle and circulating IL-15 levels. IL-15 transgenic mice ran twice as long as littermate control mice in a run-to-exhaustion trial and preferentially used fat for energy metabolism. Fast muscles in IL-15 transgenic mice exhibited high expression of intracellular mediators of oxidative metabolism that are induced by exercise, including sirtuin 1, peroxisome proliferator-activated receptor (PPAR)-δ, PPAR-γ coactivator-1α, and PPAR-γ coactivator-1β. Muscle tissue in IL-15 transgenic mice exhibited myosin heavy chain and troponin I mRNA isoform expression patterns indicative of a more oxidative phenotype than controls. These findings support a role for IL-15 in induction of exercise endurance, oxidative metabolism, and skeletal muscle molecular adaptations induced by physical training.

scholarly journals Position-specific activity of the Hox1.1 promoter in transgenic mice

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 435-442 ◽  
Author(s):  
A.W. Puschel ◽  
R. Balling ◽  
P. Gruss
Keyword(s):  
Transgenic Mice ◽  
Transgene Expression ◽  
Hox Genes ◽  
Specific Activity ◽  
Regulatory Element ◽  
Single Cells ◽  
Expression Patterns ◽  
Positional Information ◽  
Promoter Sequences ◽  
Second Period

During development, positional values have to be assigned to groups of cells. The murine Hox genes are a class of genes that are predicted to be involved at some stage in this process. During embryogenesis they are expressed in distinct overlapping region- and stage-specific patterns and therefore must be regulated in response to positional information. In this study, we have analysed the activity of Hox1.1 promoter sequences in transgenic mice. The use of lacZ as a marker allows a detailed analysis of expression at the single cell level during early embryonic development. We show that 3.6 kbp of promoter and 1.7 kbp of 3′ sequences provide sufficient regulatory information to express a transgene in a spatial and temporal manner indistinguishable from the endogenous Hox1.1 gene during the period of development when Hox1.1 expression is established. The activation occurs in a strict order in specific ectodermal and mesodermal domains. Within each of these domains the transgene is activated over a period of four hours apparently randomly in single cells. In a following second period, Hox1.1 and transgene expression patterns diverge. In this period, transgene expression persists in many mesodermally derived cells that do not express Hox1.1 indicating the absence of a negative regulatory element in the transgene. The anterior boundary of transgene expression is identical to that of Hox1.1. However, no posterior boundary of transgene expression is set, suggesting that a separate element absent from the transgene specifies this boundary.

scholarly journals How Dickkopf molecules and Wnt/beta-catenin interplay to self-organise the Hydra body axis

2021 ◽  
Author(s):  
Moritz Mercker ◽  
Alexey Kazarnikov ◽  
Anja Tursch ◽  
Suat Özbek ◽  
Thomas W Holstein ◽  
...  
Keyword(s):  
Pattern Formation ◽  
Numerical Study ◽  
Expression Patterns ◽  
Stem Cell Differentiation ◽  
Wnt Signalling ◽  
The Body ◽  
Body Axis ◽  
Beta Catenin ◽  
Mutual Inhibition ◽  
Activator Inhibitor

The antagonising interplay between canonical Wnt signalling and Dickkopf (Dkk) molecules has been identified in various processes involved in tissue organisation, such as stem cell differentiation and body-axis formation. Disruption of the interplay between these molecules is related to several diseases in humans. However, the detailed molecular mechanisms of the β-catenin/Wnt-Dkk interplay leading to robust formation of the body axis remain elusive. Although the β-catenin/Wnt signalling system has been shown in the pre-bilaterian model organism Hydra to interact with two ancestral Dkks (HyDkk1/2/4-A and -C) to self-organise and regenerate the body axis, the observed Dkk expression patterns do not match any current pattern-formation theory, such as the famous activator-inhibitor model. To explore the function of Dkk in Hydra patterning process, we propose a new mathematical model which accounts for the two Dkks in interplay with HyWnt3/β-catenin. Using a systematic numerical study, we demonstrate that the chosen set of interactions is sufficient to explain it de novo body-axis gradient formation in Hydra. The presented mutual inhibition model goes beyond the classical activator-inhibitor model and shows that a molecular mechanism based on mutual inhibition may replace the local activation/long-range inhibition loop. The new model is validated using a range of perturbation experiments. It resolves several contradictions between previous models and experimental data, and provides an explanation for the interplay between injury response and pattern formation.

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