Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The basic helix-loop-helix transcription factor Mist1 overexpression in mouse fetal hepatoblast culture

ABSTRACT: To identify the molecular mechanism of Mist1 during hepatoblasts differentiation, we performed gene expression analysis in Mist1 over-expressed cells. Dlk+ hepatoblasts derived from E13 fetal livers were purified. Purification of Dlk+ cells were performed using anti-Dlk antibody after hematopoietic cells were removed. Cells were infected with mock or Mist1-overexpressing retroviruses and cultured for 3days with oncostatin M. Virus infection was performed at the day primary culture was began (day0). Oncostatin M was added at day 1 and the cells were collected at day3. Two independent experiments were performed.

ORGANISM(S): Mus musculus

SUBMITTER: Akihide Kamiya

PROVIDER: E-GEOD-67406 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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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The basic helix-loop-helix transcription factor Mist1 overexpression in mouse fetal hepatoblast culture

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