Induced stem cell neoplasia in a cnidarian by ectopic expression of a POU domain transcription factor

Development ◽  
2011 ◽  
Vol 138 (12) ◽  
pp. 2429-2439 ◽  
Author(s):  
R. C. Millane ◽  
J. Kanska ◽  
D. J. Duffy ◽  
C. Seoighe ◽  
S. Cunningham ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Ectopic Expression ◽  
Pou Domain

scholarly journals spiel ohne grenzen/pou2is required during establishment of the zebrafish midbrain-hindbrain boundary organizer

Development ◽  
2001 ◽  
Vol 128 (21) ◽  
pp. 4165-4176 ◽  
Author(s):  
Heinz-Georg Belting ◽  
Giselbert Hauptmann ◽  
Dirk Meyer ◽  
Salim Abdelilah-Seyfried ◽  
Ajay Chitnis ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Ectopic Expression ◽  
Regional Identity ◽  
Positional Information ◽  
Neural Plate ◽  
Pou Domain ◽  
Normal Expression ◽  
Organizing Center ◽  
Wnt1 Expression ◽  
Permissive Role

The vertebrate midbrain-hindbrain boundary (MHB) organizes patterning and neuronal differentiation in the midbrain and anterior hindbrain. Formation of this organizing center involves multiple steps, including positioning of the MHB within the neural plate, establishment of the organizer and maintenance of its regional identity and signaling activities. Juxtaposition of the Otx2 and Gbx2 expression domains positions the MHB. How the positional information is translated into activation of Pax2, Wnt1 and Fgf8 expression during MHB establishment remains unclear. In zebrafish spiel ohne grenzen (spg) mutants, the MHB is not established, neither isthmus nor cerebellum form, the midbrain is reduced in size and patterning abnormalities develop within the hindbrain. In spg mutants, despite apparently normal expression of otx2, gbx1 and fgf8 during late gastrula stages, the initial expression of pax2.1, wnt1 and eng2, as well as later expression of fgf8 in the MHB primordium are reduced. We show that spg mutants have lesions in pou2, which encodes a POU-domain transcription factor. Maternal pou2 transcripts are distributed evenly in the blastula, and zygotic expression domains include the midbrain and hindbrain primordia during late gastrulation. Microinjection of pou2 mRNA can rescue pax2.1 and wnt1 expression in the MHB of spg/pou2 mutants without inducing ectopic expression. This indicates an essential but permissive role for pou2 during MHB establishment. pou2 is expressed normally in noi/pax2.1 and ace/fgf8 zebrafish mutants, which also form no MHB. Thus, expression of pou2 does not depend on fgf8 and pax2.1. Our data suggest that pou2 is required for the establishment of the normal expression domains of wnt1 and pax2.1 in the MHB primordium.

scholarly journals Low levels of Grainy head isoforms regulate Drosophila midgut intestinal stem cell differentiation

2020 ◽  
Author(s):  
Nicole Dominado ◽  
Franca Casagranda ◽  
Nicole A. Siddall ◽  
Helen E. Abud ◽  
Gary R. Hime
Keyword(s):  
Stem Cells ◽  
Transcription Factor ◽  
Stem Cell ◽  
Transcription Factors ◽  
Ectopic Expression ◽  
Stem Cell Differentiation ◽  
Intestinal Stem Cells ◽  
Stem Cell Maintenance ◽  
Low Levels ◽  
High Level

AbstractRegeneration of the Drosophila midgut epithelium depends upon differential expression of transcription factors in intestinal stem cells and their progeny. The grainy head locus produces multiple splice forms that result in production of two classes of transcription factor, designated Grh.O and Grh.N. grainy head is expressed at very low levels in the midgut and yet Grh.O is required for maintenance of intestinal stem cells and exhibits a second function regulating enteroblast differentiation in conjunction with miR-8 and Zfh-1. Grh.O expression must be tightly regulated as high level ectopic expression in enteroblasts results in cells with confused identity and promotes excess proliferation in the epithelium. Expression of Grh.N in intestinal stem cells promotes differentiation to enterocytes. Thus midgut regeneration is not only dependent upon signalling pathways that regulate transcription factor expression, but also upon regulated mRNA splicing of these genes. This study also indicates that networks of transcription factors are acting at very low levels to regulate stem cell maintenance and differentiation.

scholarly journals The Basic Helix-Loop-Helix Transcription Factor Cph2 Regulates Hyphal Development in CandidaalbicansPartly via Tec1

2001 ◽  
Vol 21 (19) ◽  
pp. 6418-6428 ◽  
Author(s):  
Shelley Lane ◽  
Song Zhou ◽  
Ting Pan ◽  
Qian Dai ◽  
Haoping Liu
Keyword(s):  
Transcription Factor ◽  
Protein Kinase ◽  
Binding Sites ◽  
Regulatory Element ◽  
Ectopic Expression ◽  
Mitogen Activated Protein Kinase ◽  
Northern Analysis ◽  
Hyphal Development ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix

ABSTRACT Candida albicans undergoes a morphogenetic switch from budding yeast to hyphal growth form in response to a variety of stimuli and growth conditions. Multiple signaling pathways, including a Cph1-mediated mitogen-activated protein kinase pathway and an Efg1-mediated cyclic AMP/protein kinase A pathway, regulate the transition. Here we report the identification of a basic helix-loop-helix transcription factor of the Myc subfamily (Cph2) by its ability to promote pseudohyphal growth inSaccharomyces cerevisiae. Like sterol response element binding protein 1, Cph2 has a Tyr instead of a conserved Arg in the basic DNA binding region. Cph2 regulates hyphal development in C. albicans, ascph2/cph2 mutant strains show medium-specific impairment in hyphal development and in the induction of hypha-specific genes. However, many hypha-specific genes do not have potential Cph2 binding sites in their upstream regions. Interestingly, upstream sequences of all known hypha-specific genes are found to contain potential binding sites for Tec1, a regulator of hyphal development. Northern analysis shows that TEC1 transcription is highest in the medium in which cph2/cph2 displays a defect in hyphal development, and Cph2 is necessary for this transcriptional induction of TEC1. In vitro gel mobility shift experiments show that Cph2 directly binds to the two sterol regulatory element 1-like elements upstream of TEC1. Furthermore, the ectopic expression of TEC1 suppresses the defect ofcph2/cph2 in hyphal development. Therefore, the function of Cph2 in hyphal transcription is mediated, in part, through Tec1. We further show that this function of Cph2 is independent of the Cph1- and Efg1-mediated pathways.

scholarly journals Chromatin and transcription factor profiling in rare stem cell populations using CUT&Tag

2021 ◽  
Vol 2 (3) ◽  
pp. 100751
Author(s):  
Yuefeng Li ◽  
Kiran Nakka ◽  
Thomas Olender ◽  
Philippe Gingras-Gelinas ◽  
Matthew Man-Kin Wong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Cell Populations ◽  
Stem Cell Populations

Proteomic analysis of transcription factor interactions in myeloid stem cell development and leukaemia

2002 ◽  
Vol 6 (4) ◽  
pp. 491-495 ◽  
Author(s):  
Gerhard Behre ◽  
Venkateshwar A Reddy ◽  
Daniel G Tenen ◽  
Wolfgang Hiddemann ◽  
Abdul A Peer Zada ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Proteomic Analysis ◽  
Cell Development ◽  
Factor Interactions

scholarly journals BRN2 is a non-canonical melanoma tumor-suppressor

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Hamm ◽  
Pierre Sohier ◽  
Valérie Petit ◽  
Jérémy H. Raymond ◽  
Véronique Delmas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Tumor Suppressor ◽  
The Other ◽  
Pi3k Signaling ◽  
Melanoma Tumor ◽  
Temporal Regulation ◽  
Metastatic Colonization ◽  
Pou Domain

AbstractWhile the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600EPtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression.

Isolation and characterization of a downstream target of Pax6 in the mammalian retinal primordium

Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 3987-3994 ◽  
Author(s):  
Gilbert Bernier ◽  
Wolfgang Vukovich ◽  
Lorenz Neidhardt ◽  
Bernhard G. Herrmann ◽  
Peter Gruss
Keyword(s):  
Transcription Factor ◽  
Expression Pattern ◽  
Large Scale ◽  
Ectopic Expression ◽  
Signal Transduction Pathway ◽  
Homeobox Gene ◽  
Optic Vesicle ◽  
Altered Expression ◽  
Retina Development ◽  
Isolation And Characterization

The transcription factor Pax6 is required for eye morphogenesis in humans, mice and insects, and can induce ectopic eye formation in vertebrate and invertebrate organisms. Although the role of Pax6 has intensively been studied, only a limited number of genes have been identified that depend on Pax6 activity for their expression in the mammalian visual system. Using a large-scale in situ hybridization screen approach, we have identified a novel gene expressed in the mouse optic vesicle. This gene, Necab, encodes a putative cytoplasmic Ca2+-binding protein and coincides with Pax6 expression pattern in the neural ectoderm of the optic vesicle and in the forebrain pretectum. Remarkably, Necab expression is absent in both structures in Pax6 mutant embryos. By contrast, the optic vesicle-expressed homeobox genes Rx, Six3, Otx2 and Lhx2 do not exhibit an altered expression pattern. Using gain-of-function experiments, we show that Pax6 can induce ectopic expression of Necab, suggesting that Necab is a direct or indirect transcriptional target of Pax6. In addition, we have found that Necab misexpression can induce ectopic expression of the homeobox gene Chx10, a transcription factor implicated in retina development. Taken together, our results provide evidence that Necab is genetically downstream of Pax6 and that it is a part of a signal transduction pathway in retina development.

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