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Glis3: The role in osteoblast differentiation and adipocyte differentiation

ABSTRACT: The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Keywords: Glis3, osteoblast differentiation, adipocyte differentiation, FGF18, BMP2

ORGANISM(S): Mus musculus

PROVIDER: GSE5379 | GEO | 2007/05/22

SECONDARY ACCESSION(S): PRJNA96285

REPOSITORIES: GEO

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Transcription profiling of mouse C3H10T1/2 cells treated with Glis3 identifies its role in osteoblast differentiation and adipocyte differentiation

Project description:The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Experiment Overall Design: Total RNA was extracted from C3H10T1/2 cells infected with empty vector or Glis3 using Qiagen Rneasy Mini kit. Each RNA sample was amplified and converted to fluorescently labeled cRNA, either with cyanine 3 (Cy3) or cyanine 5 (Cy5), using the Agilent Fluorescent Linear Amplification Kit. The fluorescently labeled cRNAs were mixed and hybridized simultaneously to Agilent mouse oligo arrays. The sample pair was hybridized to two arrays, employing a fluor reversal. Chips were scanned with an Agilent dual-laser scanner. Gene expression data were generated using the Agilent feature extraction software (v7.5), with defaults for all parameters.

2008-06-13 | E-GEOD-5379 | biostudies-arrayexpress

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GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells to Posterior Neural Progenitors

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Project description:We show that Glis3 is expressed in gonocytes, SSCs and SPCs, but not in differentiated spermatogonia or subsequent stages of spermatogenesis nor in Sertoli or Leydig cells. We further demonstrate that Glis3-deficiency causes a severe impairment in spermatogenesis in mice. Although the number of gonocytes was slightly diminished in Glis3KO testis, the number undifferentiated, PLZF+ spermatogonia was dramatically reduced leading to a virtual block in the progression of spermatogenesis. Gene expression profiling showed that the expression of a number of genes associated with self-renewal and differentiation of spermatogonial cells was significantly decreased in 1-week-old Glis3KO2 testis. These included a set of GDNF-dependent genes, such as Etv5, Bcl6b, Lhx1, Brachyury, Id4, and Pou3f1, and GDNF-independent genes, such as FoxO1, Oct4, and Zbtb16. Impairment of the nuclear localization of FoxO1 may be in part responsible for the reduced expression of Ret, Lhx1, and Sall4 in Glis3KO2 testis. Our study identifies Glis3 as a novel and critical regulator of early stages of spermatogenesis. Thy1+ cells were isolated from 3 WT and 3 Glis3KO2 testis at postnatal day 4, and total RNAs were purified from them. Then the samples were applied to Agilent mouse genome chip.

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