Determination of the zebrafish forebrain: induction and patterning

Development ◽  
1998 ◽  
Vol 125 (22) ◽  
pp. 4403-4416 ◽  
Author(s):  
Y. Grinblat ◽  
J. Gamse ◽  
M. Patel ◽  
H. Sive

We report an analysis of forebrain determination and patterning in the zebrafish Danio rerio. In order to study these events, we isolated zebrafish homologs of two neural markers, odd-paired-like (opl), which encodes a zinc finger protein, and fkh5, which encodes a forkhead domain protein. At mid-gastrula, expression of these genes defines a very early pattern in the presumptive neurectoderm, with opl later expressed in the telencephalon, and fkh5 in the diencephalon and more posterior neurectoderm. Using in vitro explant assays, we show that forebrain induction has occurred even earlier, by the onset of gastrulation (shield stage). Signaling from the early gastrula shield, previously shown to be an organizing center, is sufficient for activation of opl expression in vitro. In order to determine whether the organizer is required for opl regulation, we removed from late blastula stage embryos either the presumptive prechordal plate, marked by goosecoid (gsc) expression, or the entire organizer, marked by chordin (chd) expression. opl was correctly expressed after removal of the presumptive prechordal plate and consistently, opl was correctly expressed in one-eyed pinhead (oep) mutant embryos, where the prechordal plate fails to form. However, after removal of the entire organizer, no opl expression was observed, indicating that this region is crucial for forebrain induction. We further show that continued organizer function is required for forebrain induction, since beads of BMP4, which promotes ventral fates, also prevented opl expression when implanted during gastrulation. Our data show that forebrain specification begins early during gastrulation, and that a wide area of dorsal mesendoderm is required for its patterning.

Blood ◽  
2011 ◽  
Vol 117 (12) ◽  
pp. 3370-3381 ◽  
Author(s):  
Ingrid Saba ◽  
Christian Kosan ◽  
Lothar Vassen ◽  
Tarik Möröy

Abstract T cells originate from early T lineage precursors that have entered the thymus and differentiate through well-defined steps. Mice deficient for the BTB/POZ domain of zinc finger protein-1 (Miz-1) almost entirely lack early T lineage precursors and have a CD4−CD8− to CD4+CD8+ block causing a strong reduction in thymic cellularity. Miz-1ΔPOZ pro-T cells cannot differentiate in vitro and are unable to relay signals from the interleukin-7R (IL-7R). Both STAT5 phosphorylation and Bcl-2 up-regulation are perturbed. The high expression levels of SOCS1 found in Miz-1ΔPOZ cells probably cause these alterations. Moreover, Miz-1 can bind to the SOCS1 promoter, suggesting that Miz-1 deficiency causes a deregulation of SOCS1. Transgenic overexpression of Bcl-2 or inhibition of SOCS1 restored pro-T cell numbers and their ability to differentiate, supporting the hypothesis that Miz-1 is required for the regulation of the IL-7/IL-7R/STAT5/Bcl-2 signaling pathway by monitoring the expression levels of SOCS1.


1991 ◽  
Vol 11 (3) ◽  
pp. 1724-1728 ◽  
Author(s):  
J M Ruppert ◽  
B Vogelstein ◽  
K W Kinzler

The GLI gene was previously isolated by virtue of its amplification in human glioblastomas. We have now found that GLI expression can result in the in vitro transformation of both primary and secondary rodent cells. When coexpressed with adenovirus E1A, the GLI protein functions analogously to RAS, resulting in the formation of dense foci of cells which are tumorigenic in nude mice.


2008 ◽  
Vol 29 (3) ◽  
pp. 714-725 ◽  
Author(s):  
Melissa J. MacPherson ◽  
Linda G. Beatty ◽  
Wenjing Zhou ◽  
Minjie Du ◽  
Paul D. Sadowski

ABSTRACT The CTCF protein is a highly conserved zinc finger protein that is implicated in many aspects of gene regulation and nuclear organization. Its functions include the ability to act as a repressor of genes, including the c-myc oncogene. In this paper, we show that the CTCF protein can be posttranslationally modified by the small ubiquitin-like protein SUMO. CTCF is SUMOylated both in vivo and in vitro, and we identify two major sites of SUMOylation in the protein. The posttranslational modification of CTCF by the SUMO proteins does not affect its ability to bind to DNA in vitro. SUMOylation of CTCF contributes to the repressive function of CTCF on the c-myc P2 promoter. We also found that CTCF and the repressive Polycomb protein, Pc2, are colocalized to nuclear Polycomb bodies. The Pc2 protein may act as a SUMO E3 ligase for CTCF, strongly enhancing its modification by SUMO 2 and 3. These studies expand the repertoire of posttranslational modifications of CTCF and suggest roles for such modifications in its regulation of epigenetic states.


Chemosphere ◽  
2009 ◽  
Vol 77 (7) ◽  
pp. 928-933 ◽  
Author(s):  
René Schreiber ◽  
Rolf Altenburger ◽  
Albrecht Paschke ◽  
Gerrit Schüürmann ◽  
Eberhard Küster

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Morgan Salmon ◽  
Nicolas H Pope ◽  
William F Johnston ◽  
John P Davis ◽  
Gary K Owens ◽  
...  

Objective: Previously, we found that the zinc-finger protein 148(ZFP148) binds to smooth muscle(SMC) genes following ligation injury; however, it has no known role in aortic aneurysm formation. The study objective was to determine whether ZFP148 is important in AA formation. Methods: ZFP148 was examined via qPCR in human aortic aneurysms(n=12/group). 8-12 week male C57/B6 mice (n=6/group) underwent elastase perfusion and were harvested at 3, 7, and 14 days for qPCR for ZFP148. Separately, 8-12 week male (n=10/group) ZFP flx/flx Myh11 Cre+(SMC tamoxifen ZFP148 KO), Myh11 ZFP148 flx/wt Cre+ and Myh11 ZFP wt/wt Cre+ underwent elastase perfusion. At 14 days, maximal aortic dilation was measured with video micrometry. ZFP148 flx/flx ERT Cre+ (n=10/group) and ZFP148 flx/flx ERT Cre-(WT) mice also underwent elastase perfusion. A separate set of mice were bred to an ApoE-/- background and administered Angiotensin II via osmotic pump. Aortic samples were evaluated with histology for α-actin, macrophages, neutrophils, T lymphocytes, caspase3, Ki67, and elastin. In vitro ZFP148 was knocked down using siRNA in smooth muscle cells and stimulated with elastase, or IL-1β. Results: ZFP148 expression was elevated in human and murine AA. Maximal aortic dilation was significantly reduced in SMC ZFP148 KO mice compared with controls (55.7 ± 6.32% versus 106.4 ± 8.43%, p<0.05). Maximal aortic dilation of ERT Cre+ ZFP148 mice was significantly decreased versus WT controls (50.4± 8.65% versus 101.3± 9.43%, p<0.05). Knock-out of ZFP148 in both elastase models demonstrated reduced macrophage, T-cell, Ki-67, Caspase3 and neutrophil staining. Kaplan-Meier curves demonstrated increased survival in SM-MHC ZFP148 flx/flx (Chi2=4.357, p=0.0421) and flx/wt mice (Chi2=4.169, p=0.0476) compared to their WT controls following Angiotensin II infusion. Knock-down of ZFP148 followed by treatment with elastase or IL-1β in SMCs attenuated the down-regulation of SM22α, SM-MHC, and SMαA. ZFP148 bound via ChIP analysis to SMC marker genes in vitro and in vivo and was found to bind within the proximal promoter region of SmαA and SM22α. Conclusions: ZFP148 KO attenuates AA formation and binds to smooth muscle marker genes. ZFP148 could represent a novel regulator of vascular disease.


2009 ◽  
Vol 221 (3) ◽  
pp. 771-777 ◽  
Author(s):  
Valentina Rossi ◽  
Stefania Staibano ◽  
Ciro Abbondanza ◽  
Daniela Pasquali ◽  
Caterina De Rosa ◽  
...  

2004 ◽  
Vol 319 (1) ◽  
pp. 169-177 ◽  
Author(s):  
Patrı́cia A Mörking ◽  
Bruno M Dallagiovanna ◽  
Leonardo Foti ◽  
Beatriz Garat ◽  
Gisele F.A Picchi ◽  
...  

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Fengwei Li ◽  
Qinjunjie Chen ◽  
Hui Xue ◽  
Lei Zhang ◽  
Kui Wang ◽  
...  

Abstract Long non-coding RNAs (lncRNAs) have extremely complex roles in the progression of intrahepatic cholangiocarcinoma (ICC) and remain to be elucidated. By cytological and animal model experiments, this study demonstrated that the expression of lncRNA MNX1-AS1 was remarkably elevated in ICC cell lines and tissues, and was highly and positively correlated with motor neuron and pancreas homeobox protein 1 (MNX1) expression. MNX1-AS1 significantly facilitated the proliferation, migration, invasion, and angiogenesis in ICC cells in vitro, and remarkably promoted tumor growth and metastasis in vivo. Further study revealed that MNX1-AS1 promoted the expression of MNX1 via recruiting transcription factors c-Myc and myc-associated zinc finger protein (MAZ). Furthermore, MNX1 upregulated the expression of Ajuba protein via binding to its promoter region, and subsequently, Ajuba protein suppressed the Hippo signaling pathway. Taken together, our results uncovered that MNX1-AS1 can facilitate ICC progression via MNX1-AS1/c-Myc and MAZ/MNX1/Ajuba/Hippo pathway, suggesting that MNX1-AS1 may be able to serve as a potential target for ICC treatment.


Protist ◽  
2010 ◽  
Vol 161 (3) ◽  
pp. 489-496 ◽  
Author(s):  
Guanghan Gao ◽  
Kestrel Rogers ◽  
Feng Li ◽  
Qiang Guo ◽  
Daren Osato ◽  
...  

1990 ◽  
Vol 10 (5) ◽  
pp. 1931-1939
Author(s):  
X M Cao ◽  
R A Koski ◽  
A Gashler ◽  
M McKiernan ◽  
C F Morris ◽  
...  

Egr-1 is an immediate-early response gene induced by diverse signals that initiate growth and differentiation. Its cDNA sequence predicts a protein with zinc fingers. We have generated an antiserum to the Egr-1 gene product and identified it as an 80-kilodalton short-lived protein in serum-stimulated mouse fibroblasts. The rat Egr-1 product has also been identified in nerve growth factor-induced PC12 cells. In addition, we show by cell fractionation and immunocytochemistry that the Egr-1 protein is located in the nucleus. We also demonstrate that it is phosphorylated. In vitro-generated Egr-1 protein binds with high affinity to the sequence CGCCCCCGC in a zinc-dependent manner.


Sign in / Sign up

Export Citation Format

Share Document