scholarly journals miR-183/96/182 cluster is an important morphogenetic factor targeting PAX6 expression in differentiating human retinal organoids

Stem Cells ◽  
2020 ◽  
Author(s):  
Lucie Peskova ◽  
Denisa Jurcikova ◽  
Tereza Vanova ◽  
Jan Krivanek ◽  
Michaela Capandova ◽  
...  
Keyword(s):  
Pax6 Expression

Pax6 expression highlights regional organization in the adult brain of lungfishes, the closest living relatives of land vertebrates

2019 ◽  
Vol 528 (1) ◽  
pp. 139-163
Author(s):  
Jesús M. López ◽  
Ruth Morona ◽  
Nerea Moreno ◽  
Daniel Lozano ◽  
Sara Jiménez ◽  
...  
Keyword(s):  
Adult Brain ◽  
Pax6 Expression ◽  
Regional Organization ◽  
Land Vertebrates

The upstream ectoderm enhancer in Pax6 has an important role in lens induction

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4415-4424 ◽  
Author(s):  
Patricia V. Dimanlig ◽  
Sonya C. Faber ◽  
Woytek Auerbach ◽  
Helen P. Makarenkova ◽  
Richard A. Lang
Keyword(s):  
Transcriptional Control ◽  
Control Element ◽  
Pax6 Gene ◽  
Pax6 Expression ◽  
Surface Ectoderm ◽  
Targeted Deletion ◽  
Lens Vesicle ◽  
Normal Lens ◽  
Lens Formation ◽  
Lens Placode

The Pax6 gene has a central role in development of the eye. We show, through targeted deletion in the mouse, that an ectoderm enhancer in the Pax6 gene is required for normal lens formation. Ectoderm enhancer-deficient embryos exhibit distinctive defects at every stage of lens development. These include a thinner lens placode, reduced placodal cell proliferation, and a small lens pit and lens vesicle. In addition, the lens vesicle fails to separate from the surface ectoderm and the maturing lens is smaller and shows a delay in fiber cell differentiation. Interestingly, deletion of the ectoderm enhancer does not eliminate Pax6 production in the lens placode but results in a diminished level that, in central sections, is apparent primarily on the nasal side. This argues that Pax6 expression in the lens placode is controlled by the ectoderm enhancer and at least one other transcriptional control element. It also suggests that Pax6 enhancers active in the lens placode drive expression in distinct subdomains, an assertion that is supported by the expression pattern of a lacZ reporter transgene driven by the ectoderm enhancer. Interestingly, deletion of the ectoderm enhancer causes loss of expression of Foxe3, a transcription factor gene mutated in the dysgenetic lens mouse. When combined, these data and previously published work allow us to assemble a more complete genetic pathway describing lens induction. This pathway features (1) a pre-placodal phase of Pax6 expression that is required for the activity of multiple, downstream Pax6 enhancers; (2) a later, placodal phase of Pax6 expression regulated by multiple enhancers; and (3) the Foxe3 gene in a downstream position. This pathway forms a basis for future analysis of lens induction mechanism.

FGF signalling controls the timing of Pax6 activation in the neural tube

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4837-4843 ◽  
Author(s):  
N. Bertrand ◽  
F. Medevielle ◽  
F. Pituello
Keyword(s):  
Spinal Cord ◽  
Neural Tube ◽  
Inhibitory Activity ◽  
Neural Plate ◽  
Presomitic Mesoderm ◽  
Pax6 Expression ◽  
Epithelial Development ◽  
Repressive Effect ◽  
Caudal Regression ◽  
Fgf Signalling

We have recently demonstrated that Pax6 activation occurs in phase with somitogenesis in the spinal cord. Here we show that the presomitic mesoderm exerts an inhibitory activity on Pax6 expression. This repressive effect is mediated by the FGF signalling pathway. The presomitic mesoderm displays a decreasing caudorostral gradient of FGF8, and grafting FGF8-soaked beads at the level of the neural tube abolishes Pax6 activation. Conversely, when FGF signalling is disrupted, Pax6 is prematurely activated in the neural plate. We propose that the progression of Pax6 activation in the neural tube is controlled by the caudal regression of the anterior limit of FGF activity. Hence, as part of its posteriorising activity, FGF8 downregulation acts as a switch from early (posterior) to a later (anterior) state of neural epithelial development.

PAX6 expression may be protective against dopaminergic cell loss in Parkinson's disease

2016 ◽  
Vol 15 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Meghan G. Thomas ◽  
Caitlyn Welch ◽  
Leah Stone ◽  
Peter Allan ◽  
Roger A. Barker ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Loss ◽  
Pax6 Expression ◽  
Dopaminergic Cell

scholarly journals Long-range downstream enhancers are essential for Pax6 expression

2006 ◽  
Vol 299 (2) ◽  
pp. 563-581 ◽  
Author(s):  
Dirk A. Kleinjan ◽  
Anne Seawright ◽  
Sebastien Mella ◽  
Catherine B. Carr ◽  
David A. Tyas ◽  
...  
Keyword(s):  
Long Range ◽  
Pax6 Expression

scholarly journals Regulation of Human PAX6 Expression by miR-7

2014 ◽  
Vol 10 ◽  
pp. EBO.S13739 ◽  
Author(s):  
Maria Needhamsen ◽  
Robert B. White ◽  
Keith M. Giles ◽  
Sarah A. Dunlop ◽  
Meghan G. Thomas
Keyword(s):  
Pax6 Expression

scholarly journals Spatial specification of mammalian eye territories by reciprocal transcriptional repression of Pax2 and Pax6

Development ◽  
2000 ◽  
Vol 127 (20) ◽  
pp. 4325-4334 ◽  
Author(s):  
M. Schwarz ◽  
F. Cecconi ◽  
G. Bernier ◽  
N. Andrejewski ◽  
B. Kammandel ◽  
...  
Keyword(s):  
Visual System ◽  
Transcriptional Repression ◽  
Ectopic Expression ◽  
Pax6 Gene ◽  
Loss Of Function ◽  
Pax6 Expression ◽  
Expression Domain ◽  
Enhancer Activity ◽  
Optic Stalk ◽  
Optic Cup

We have studied the molecular basis of the Pax2 and Pax6 function in the establishment of visual system territories. Loss-of-function mutants have revealed crucial roles for Pax2 in the generation of the optic stalk and for Pax6 in the development of the optic cup. Ectopic expression of Pax6 in the optic stalk under control of Pax2 promoter elements resulted in a shift of the optic cup/optic stalk boundary indicated by the presence of retinal pigmented cells on the optic stalk. By studying mouse embryos at early developmental stages we detected an expansion of Pax2 expression domain in the Pax6(−/−) mutant and of Pax6 expression domain in the Pax2(−/−) embryo. These results suggest that the position of the optic cup/optic stalk boundary depends on Pax2 and Pax6 expression, hinting at a possible molecular interaction. Using gel shift experiments, we confirmed the presence of Pax2- and Pax6-binding sites on the retina enhancer of the Pax6 gene and on the Pax2 upstream control region, respectively. Co-transfection experiments revealed a reciprocal inhibition of Pax2 promoter/enhancer activity by Pax6 protein and vice versa. Based on our findings, we propose a model for Pax gene regulation that establishes the proper spatial regionalization of the mammalian visual system.

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