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Endogenous beta-galactosidase activity marks TREM2-expressing Kupffer cell population in the livers of carbon tetrachloride-treated Lgr5-LacZ mice

ABSTRACT: Lgr5+ cells isolated from liver organoids act as bipotent liver progenitors. Beta-galactosidase (beta-gal)-expressing cells appear in injured livers of Lgr5-LacZ mice, however, their origin and identity has remained controversial. Here we sought to clarify this issue. The majority of beta-gal+ cells emerged in pericentral regions of the liver lobule. Lineage tracing demonstrated that beta-gal+ cells did not originate from hepatocytes or cholangiocytes. Beta-gal+ cells were negative for hepatocyte and cholangiocyte markers; but positive for Kupffer cell markers. Transcriptome analysis revealed the expression of endogenous beta-galactosidase Glb1 and genes characteristic of TREM2+ macrophages that may regulate stem cell maintenance. We were not able to detect the expression of the Lgr5-LacZ transgene and concluded that the transgene was silenced.

ORGANISM(S): Mus musculus

PROVIDER: GSE132206 | GEO | 2019/11/14

REPOSITORIES: GEO

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Project description:Liebal2012 - B.subtilis post-transcription instability model An important transcription factor of B.subsilis is sigma B . Liebal et al. (2012) have performed experiments in B.subtilis wild type and mutant straits to test and validate a mathematical model of the dynamics of sigma B activity. The following three models were constructed and their ability to fit the experimental data were tested. 1) Transcription inhibition model (MODEL1212180000), 2) sigma B proteolysis model (MODEL1302080000) and 3) Post-transcriptional instability model (MODEL1302080001). This model corresponds to the post-transcription instability model (MODEL1302080001). This model is described in the article: Proteolysis of beta-galactosidase following SigmaB activation in Bacillus subtilis. Liebal UW, Sappa PK, Millat T, Steil L, Homuth G, Völker U, Wolkenhauer O. 2012 Jun;8(6):1806-14. Abstract: In Bacillus subtilis the σ(B) mediated general stress response provides protection against various environmental and energy related stress conditions. To better understand the general stress response, we need to explore the mechanism by which the components interact. Here, we performed experiments in B. subtilis wild type and mutant strains to test and validate a mathematical model of the dynamics of σ(B) activity. In the mutant strain BSA115, σ(B) transcription is inducible by the addition of IPTG and negative control of σ(B) activity by the anti-sigma factor RsbW is absent. In contrast to our expectations of a continuous β-galactosidase activity from a ctc::lacZ fusion, we observed a transient activity in the mutant. To explain this experimental finding, we constructed mathematical models reflecting different hypotheses regarding the regulation of σ(B) and β-galactosidase dynamics. Only the model assuming instability of either ctc::lacZ mRNA or β-galactosidase protein is able to reproduce the experiments in silico. Subsequent Northern blot experiments revealed stable high-level ctc::lacZ mRNA concentrations after the induction of the σ(B) response. Therefore, we conclude that protein instability following σ(B) activation is the most likely explanation for the experimental observations. Our results thus support the idea that B. subtilis increases the cytoplasmic proteolytic degradation to adapt the proteome in face of environmental challenges following activation of the general stress response. The findings also have practical implications for the analysis of stress response dynamics using lacZ reporter gene fusions, a frequently used strategy for the σ(B) response. Figure 3a of the reference article has been reproduced. beta-galactosidase (lacz in model) activity at different concentrations of IPTG (100M, 200M and 1000M) has been reproduced. SED-ML (Simulation Experiment Description Markup Language) file is available for this model (see curation tab). This model is hosted on BioModels Database and identified by: MODEL1302080001 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Endogenous beta-galactosidase activity marks TREM2-expressing Kupffer cell population in the livers of carbon tetrachloride-treated Lgr5-LacZ mice

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