ATBF1‐A protein, but not ATBF1‐B, is preferentially expressed in developing rat brain

Ikoma, Yoko; Kikuchi, Makoto; Takagawa, Kiyoshi; Oya, Takeshi; Nogami, Shigeharu; Tamura, Akio; Miura, Yutaka; Ido, Akio; Sakata, Nobuo; Hashimoto-Tamaoki, Tomoko; Kimura, Takeshi; Saito, Takayoshi; Tamaoki, Taiki; Sasahara, Masakiyo

doi:10.1002/cne.10807

Cited by 31 publications

(34 citation statements)

References 54 publications

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“…The peptide characterized in the proteomic analysis corresponded to the 404-kDa isoform that contains four homeodomains and 23 zinc fingers (16). Atbf1 mRNA is highly expressed in the developing brain (17). In the mouse, its expression peaks around E13-E15 and progressively decreases to an undetectable level by postnatal day 28 (18).…”

Section: Identification Of Atbf1 As the Main Ee␣ Binding Factor By Qumentioning

confidence: 99%

Atbf1 is required for the Pit1 gene early activation

Ranish

Zhu

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Enhancers have been functionally described for >35 years, but the molecular principles underlying the integration of regulatory inputs to alternate gene enhancers used during mammalian organogenesis remain incompletely understood. Using a combination of in vivo enhancer mapping and proteomics approaches, we have established that two distant and distinct early enhancers, each requiring different transcription complexes, are required for full activation of the gene encoding the pituitary lineage determining factor, Pit1. A transcription factor belonging to the ''giant, multiple-homeodomain and zinc finger family,'' Atbf1, serves as a novel pituitary regulator for one of the two required enhancers as shown by genetic and in vitro analysis.T he essence of embryonic development is to generate a regulated increase in cell number and diversity, with the identity of each cell type dictated by specific patterns of signals and expression of sets of genes Thus, a hierarchy of regulatory factors controls activation or repression of such genes with spatial/temporal precision, and such control is central to accurately unfolding genetic information to create precise patterns of developmental complexity. It involves evolutionarily conserved cis-regulatory sequences that are highly structured and organized to recruit sets of transcription activators/ repressors. These transcription complexes will determine the rate and frequency of transcription initiation, generating fine control of gene expression in development, homeostasis, and disease.The anterior pituitary gland provides an excellent model system to analyze molecular programs governing cell-specific gene regulation during embryonic development. The mature pituitary gland contains five distinct hormone-producing cell types: corticotropes, somatotropes, lactotropes, thyrotropes, and gonadotropes. All of these cell types arise from a common primordium, the Rathke's pouch, which initially develops by mouse embryonic day 9 (E9) as a single layer of epithelium; it undergoes a fast expansion attributable to intense cell proliferation and gives rise to a series of cell lineages, which eventually develop into the five cell types in response to precise spatial/temporal patterns of overlapping signaling gradients and involves several transcription factors (reviewed in refs. 1-6). Pit1, a POU-homeodomain transcription factor, is the lineage regulator responsible for the generation of somatotropes, lactotropes, and thyrotropes (7). Pit1 expression is initiated by E13.5 and is maintained in adulthood, being directly involved in the transcriptional control of the genes encoding growth hormone (GH), prolactin (Prl), and thyroid-stimulating hormone (TSH␤) (8). Our previous studies revealed that 14.8 kb of 5Ј-flanking sequence of the Pit1 gene was sufficient to direct the robust expression of a reporter in an identical spatial and temporal pattern as endogenous Pit1, whereas its minimal promoter (Ϫ327 bp to ϩ13 bp) was insufficient to drive detectable reporter expression in transgenic mice ...

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Section: Identification Of Atbf1 As the Main Ee␣ Binding Factor By Qumentioning

confidence: 99%

Atbf1 is required for the Pit1 gene early activation

Ranish

Zhu

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…After inhibition of endogenous peroxidase activity by immersion in 3% H 2 O 2 /methanol solution, antigen retrieval was conducted for detection of binding of the undermentioned antibodies with 10 mmol/l citrate buffer (pH 6.0) in a microwave oven for 10 min at 98°C. Sections were incubated with primary antibodies against ATBF1 27 or MUC5AC (Novocastra Laboratories, Newcastle, UK), 4 thoroughly washed in phosphate-buffered solution (PBS), then incubated with biotinylated secondary antibody followed by avidin-biotinylated horseradish peroxidase complex (Vectastain Elite ABC kit, Vector Laboratories, Burlingame, CA). Finally, immune complexes were visualized by incubation with 0.01% H 2 O 2 and 0.05% 3,3 0 -diaminobenzidine tetrachloride (DAB).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Subcellular localization of ATBF1 regulates MUC5AC transcription in gastric cancer

Mori

Kataoka

Miura

et al. 2007

Intl Journal of Cancer

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Human gastric epithelium has a unique mucin gene expression pattern, which becomes markedly altered in gastrointestinal disorder. This alteration in mucin expression, including the mucin MUC5AC, may be related to the development and prognosis of gastric cancers, and MUC5AC-positive gastric cancer has been reported to be poor prognosis. However, the molecular mechanism of MUC5AC transcriptional regulation has not been fully elucidated. AT motif-binding factor 1 (ATBF1) is a homeotic transcriptional regulatory factor recently identified as a tumor suppressor gene, and its subcellular localization suggests a link to cell proliferation and differentiation. We investigated the mechanism of MUC5AC transcriptional regulation by ATBF1. In 123 gastric cancer lesions, ATBF1 expressed in the nucleus significantly suppressed MUC5AC expression, as determined by immunohistochemistry. In addition, analysis of the MUC5AC promoter region revealed an AT motif-like element. This element was found to be essential for ATBF1 suppression of MUC5AC promoter activity as shown in a dual luciferase-reporter assay. Over-expressed ATBF1 also significantly suppressed endogenous MUC5AC protein expression in gastric cancer cells. Chromatin immunoprecipitation demonstrated that ATBF1 binds to the AT motif-like element in the MUC5AC promoter. These results indicate that ATBF1 in the nucleus negatively regulates the MUC5AC gene in gastric cancer by binding to an AT motif-like element in the MUC5AC promoter. ' 2007 Wiley-Liss, Inc.

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“…Glass-mounted 4 m sections were deparaffinized and rehydrated, and the antigens were reactivated in 0.01 M citrate buffer (pH 6.0) at 110°C for 5 minutes. Incubation with primary antibodies against ATBF1 (D1-120; MBL) (Ishii et al, 2003), BrdU (5-bromo-2Ј-deoxy-uridine labeling and detection kit I; Roche), nestin (MAB353; Chemicon), ␤-tubulin III (T8660; Sigma) or proliferating cell nuclear antigen (Clone PC10; Dako Cytomation) was generally performed in a solution of phosphate-buffered saline containing 1% goat serum and 0.25% Triton X-100 at room temperature for 1 hour. The secondary antibodies were Alexa 594-conjugated goat anti-rabbit IgG and Alexa 488-conjugated goat anti-mouse IgG (Molecular Probes).…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…An ATBF1 ortholog in Drosophila, Zfh2, binds to an AT-rich element located upstream of the DOPA decarboxylase (Ddc) gene responsible for specific neuronal differentiation of the central nervous system (CNS) (Lundell and Hirsh, 1992) and to an opsin regulatory element responsible for differentiation of the lens (Fortini et al, 1991), suggesting that ATBF1 is involved in neuronal differentiation. Previously, we have characterized a full-length cDNA of Atbf1 and showed that it is highly expressed in the CNS and dopaminergic neurons in a neuronal differentiation-dependent manner (Miura et al, 1995;Ishii et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Homeotic factor ATBF1 induces the cell cycle arrest associated with neuronal differentiation

Jung

Kim

Kikuchi³

et al. 2005

Development

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The present study aimed to elucidate the function of AT motif-binding factor 1 (ATBF1) during neurogenesis in the developing brain and in primary cultures of neuroepithelial cells and cell lines (Neuro 2A and P19 cells). Here, we show that ATBF1 is expressed in the differentiating field in association with the neuronal differentiation markers β-tubulin and MAP2 in the day E14.5 embryo rat brain, suggesting that it promotes neuronal differentiation. In support of this, we show that ATBF1 suppresses nestin expression, a neural stem cell marker, and activates the promoter of Neurod1 gene, a marker for neuronal differentiation. Furthermore, we show that in Neuro 2A cells, overexpressed ATBF1 localizes predominantly in the nucleus and causes cell cycle arrest. In P19 cells, which formed embryonic bodies in the floating condition, ATBF1 is mainly cytoplasmic and has no effect on the cell cycle. However, the cell cycle was arrested when ATBF1 became nuclear after transfer of P19 cells onto adhesive surfaces or in isolated single cells. The nuclear localization of ATBF1 was suppressed by treatment with caffeine, an inhibitor of PI(3)K-related kinase activity of ataxa-telangiectasia mutated (ATM) gene product. The cytoplasmic localization of ATBF1 in floating/nonadherent cells is due to CRM1-dependent nuclear export of ATBF1. Moreover, in the embryonic brain ATBF1 was expressed in the cytoplasm of proliferating stem cells on the ventricular zone, where cells are present at high density and interact through cell-to-cell contact. Conversely,in the differentiating field, where cell density is low and extracellular matrix is dense, the cell-to-matrix interaction triggered nuclear localization of ATBF1, resulting in the cell cycle arrest. We propose that ATBF1 plays an important role in the nucleus by organizing the neuronal differentiation associated with the cell cycle arrest.

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ATBF1‐A protein, but not ATBF1‐B, is preferentially expressed in developing rat brain

Cited by 31 publications

References 54 publications

Atbf1 is required for the Pit1 gene early activation

Atbf1 is required for the Pit1 gene early activation

Subcellular localization of ATBF1 regulates MUC5AC transcription in gastric cancer

Homeotic factor ATBF1 induces the cell cycle arrest associated with neuronal differentiation

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