Mouse Mist1 and Lrig1 apc tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA804102 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17913159_1.fastq.gz | Fastqsanger.gz | |||
| SRR17913159_2.fastq.gz | Fastqsanger.gz | |||
| SRR17913160_1.fastq.gz | Fastqsanger.gz | |||
| SRR17913160_2.fastq.gz | Fastqsanger.gz | |||
| SRR17913161_1.fastq.gz | Fastqsanger.gz |
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Project description:MIST1 over-expression has not been analyzed in a cell type that does not express endogenous MIST1. Here, we force-express ectopic MIST1 in the hepatocytes of mouse livers. We extracted mRNA and compared gene expression levels between MIST1-expressing mouse livers to controls.
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Project description:MIST1 over-expression has not been analyzed in a cell type that does not express endogenous MIST1. Here, we force-express ectopic MIST1 in the parietal cells of mouse stomachs. We extracted whole corpus stomach mRNA and compared gene expression levels between MIST1-expressing mouse stomachs to controls.
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Project description:Mist1+ cells and parietal cells in mouse stomach were separatedly sorted, and RNAs were isolated. Mist1 (also known as Bhlha15) is expressed in gastric chief cells and gastric stem cells in mice. However, more specific genes for each population needs to be identified to better understand the precise biology in these cell populations. In order to address cell specific gene signature, we separately sorted Mist1+ gastric chief cells and Mist1+ gastric stem cells by FACS, and performed microarray analysis. Mist1+ gastric chief cells were sorted by using Mist1-CreERT; R26-TdTomato mouse stomach, immediately after tamoxifen administration. Mist1+ gastric stem cells were sorted by chief cell-ablated Mist1-CreERT; R26-TdTomato mouse stomach, combining with Lgr5-DTR mice. Lgr5-expressing chief cells were ablated by giving DT into these mice. As a control, acid-secreting gastric parietal cell samples were used. Mice were treated with or without Lgr5-DT ablation before sorting.
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Project description:Although early developmental processes involve cell fate decisions that define the body axes and establish progenitor cell pools, development does not cease once cells are specified. Instead, most cells undergo specific maturation events where changes in the cell transcriptome ensure that the proper gene products are expressed to carry out unique physiological functions. Pancreatic acinar cells mature post-natally to handle an extensive protein synthetic load, establsih organized apical-basal polarity for zymogen granule trafficking, and assemble gap-junctions to perimt efficient cell-cell communication. Despite significant progress in defining transcriptional networks that control initial acinar cell specification and differentiation decisions, little is know regarding the role of transcription factors in the specification and maintenance of maturation events. One candidate maturation effector is MIST1, a secretory cell-restricted transcription factor that has been implicated in controlling regulated exocytosis events in a number of cell types. Embryonic knock-out of MIST1 generates acinar cells that fail to establish an apical-basal organization, fail to properly localize zymogen granule and fail to communicate intra-cellularly, making the exocrine organ highly suceptible to pancreatic diseases. In an effort to identify the gene expression differences responsible for MIST1 regulating mature acinar properties. We generated a tamoxifen-inducible mouse model where MIST1 expression could be activated in vivoand performed gene expression arrays on wildtype, MIST1-null, and induced MIST1 pancreatic RNA. RNA was isolated from pancreata of 8 week old mice using the Qiagen RNeasy Midi kit. Pancreta of wildtype, MIST1-null, and MIST1-null with a tamoxifen inducible MIST1-expressing transgene were harvested 36 hours post-tamoxifen administration. Therefore, this experiment provides information on steady-state gene expression differences between wildtype and MIST1-null mice as well as immediate gene expression changes induced by MIST1 expression.
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Project description:Mist1+CD24hi cells and Mist1+CD24lo cells in mouse small intestine were separatedly sorted, and RNAs were isolated. Mice were treated with irradiation, Lgr5-DT ablation, doxorubicin, or NICD expression before sorting.
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Project description:RNA-seq analysis of Lrig1+ and Lrig1- CD4+ T cells in mouse spleen
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