A novel fork head gene mediates early steps during Xenopus lens formation

Development ◽  
1999 ◽  
Vol 126 (22) ◽  
pp. 5107-5116
Author(s):  
K.L. Kenyon ◽  
S.A. Moody ◽  
M. Jamrich
Keyword(s):  
Neural Plate ◽  
Gene Products ◽  
Fork Head ◽  
Undifferentiated State ◽  
Temporal And Spatial ◽  
Differentiation Marker ◽  
Lens Formation ◽  
Lens Placode ◽  
Fork Head Gene ◽  
Anterior Neural Plate

Xlens1 is a novel Xenopus member of the fork head gene family, named for its nearly restricted expression in the anterior ectodermal placode, presumptive lens ectoderm (PLE), and anterior epithelium of the differentiated lens. The temporal and spatial restriction of its expression suggests that: (1) Xlens1 is transcribed initially at neural plate stages in response to putative signals from the anterior neural plate that transform lens-competent ectoderm to lens-biased ectoderm; (2) further steps in the process of lens-forming bias restrict Xlens1 expression to the presumptive lens ectoderm (PLE) during later neural plate stages; (3) interactions with the optic vesicle maintain Xlens1 expression in the lens placode; and (4) Xlens1 expression is downregulated as committed lens cells undergo terminal differentiation. Induction assays demonstrate that pax6 induces Xlens1 expression, but unlike pax6, Xlens1 cannot induce the expression of the lens differentiation marker beta-crystallin. In the whole embryo, overexpression of Xlens1 in the lens ectoderm causes it to thicken and maintain gene expression characteristics of the PLE. Also, this overexpression suppresses differentiation in the lens ectoderm, suggesting that Xlens1 functions to maintain specified lens ectoderm in an undifferentiated state. Misexpression of Xlens1 in other regions causes hypertrophy of restricted tissues but only occasionally leads ectopic sites of gamma-crystallin protein expression in select anterior head regions. These results indicate that Xlens1 expression alone does not specify lens ectoderm. Lens specification and differentiation likely depends on a combination of other gene products and an appropriate level of Xlens1 activity.

Gene activation during early stages of lens induction in Xenopus

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3509-3519 ◽  
Author(s):  
C.A. Zygar ◽  
T.L. Cook ◽  
R.M. Grainger
Keyword(s):  
Neural Tube ◽  
Gene Activation ◽  
Neural Plate ◽  
Neural Tube Closure ◽  
Gene Products ◽  
Optic Vesicle ◽  
Determination Process ◽  
Tightly Coupled ◽  
Anterior Neural Plate ◽  
Tube Closure

Several stages in the lens determination process have been defined, though it is not known which gene products control these events. At mid-gastrula stages in Xenopus, ectoderm is transiently competent to respond to lens-inducing signals. Between late gastrula and neural tube stages, the presumptive lens ectoderm acquires a lens-forming bias, becomes specified to form lens and begins differentiation. Several genes have been identified, either by expression pattern, mutant phenotype or involvement in crystallin gene regulation, that may play a role in lens bias and specification, and we focus on these roles here. Fate mapping shows that the transcriptional regulators Otx-2, Pax-6 and Sox-3 are expressed in the presumptive lens ectoderm prior to lens differentiation. Otx-2 appears first, followed by Pax-6, during the stages of lens bias (late neural plate stages); expression of Sox-3 follows neural tube closure and lens specification. We also demonstrate the expression of these genes in competent ectoderm transplanted to the lens-forming region. Expression of these genes is maintained or activated preferentially in ectoderm in response to the anterior head environment. Finally, we examined activation of these genes in response to early and late lens-inducing signals. Activation of Otx-2, Pax-6 and Sox-3 in competent ectoderm occurs in response to the early inducing tissue, the anterior neural plate. Since Sox-3 is activated following neural tube closure, we tested its dependence on the later inducing tissue, the optic vesicle, which contacts lens ectoderm at this stage. Sox-3 is not expressed in lens ectoderm, nor does a lens form, when the optic vesicle anlage is removed at late neural plate stages. Expression of these genes demarcates patterning events preceding differentiation and is tightly coupled to particular phases of lens induction.

scholarly journals Evolution of Mouse T-box Genes by Tandem Duplication and Cluster Dispersion

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 249-254 ◽  
Author(s):  
Sergei I Agulnik ◽  
Nancy Garvey ◽  
Sarah Hancock ◽  
Ilya Ruvinsky ◽  
Deborah L Chapman ◽  
...  
Keyword(s):  
Tandem Duplication ◽  
Crossing Over ◽  
Dna Binding Domain ◽  
Gene Products ◽  
New Members ◽  
Ancestral Gene ◽  
T Box ◽  
Temporal And Spatial Patterns ◽  
Temporal And Spatial ◽  
T Locus

Abstract The T-box genes comprise an ancient family of putative transcription factors conserved across species as divergent as Mus musculus and Caenorhabditis elegans. All T-box gene products are characterized by a novel 174-186amino acid DNA binding domain called the T-box that was first discovered in the polypeptide products of the mouse T locus and the Drosophila melanogaster optomotor-blind gene. Earlier studies allowed the identification of five mouse T-box genes, T, Tbx1-3, and Tbr1, that all map to different chromosomal locations and are expressed in unique temporal and spatial patterns during embryogenesis. Here, we report the discovery of three new members of the mouse T-box gene family, named Tbx4, Tbx5, and Tbx6. Two of these newly discovered genes, Tbx4 and Tbx5, were found to be tightly linked to previously identified T-box genes. Combined results from phylogenetic, linkage, and physical mapping studies provide a picture for the evolution of a T-box subfamily by unequal crossing over to form a two-gene cluster that was duplicated and dispersed to two chromosomal locations. This analysis suggests that Tbx4 and Tbx5 are cognate genes that diverged apart from a common ancestral gene during early vertebrate evolution.

scholarly journals Hallmarks of primary neurulation are conserved in the zebrafish forebrain

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Jonathan M. Werner ◽  
Maraki Y. Negesse ◽  
Dominique L. Brooks ◽  
Allyson R. Caldwell ◽  
Jafira M. Johnson ◽  
...  
Keyword(s):  
Neural Tube ◽  
Time Lapse ◽  
Neural Plate ◽  
Neural Tube Closure ◽  
Developmental Studies ◽  
Underlying Causes ◽  
The Central Nervous System ◽  
Resolution Imaging ◽  
Fold Formation ◽  
Anterior Neural Plate

AbstractPrimary neurulation is the process by which the neural tube, the central nervous system precursor, is formed from the neural plate. Incomplete neural tube closure occurs frequently, yet underlying causes remain poorly understood. Developmental studies in amniotes and amphibians have identified hingepoint and neural fold formation as key morphogenetic events and hallmarks of primary neurulation, the disruption of which causes neural tube defects. In contrast, the mode of neurulation in teleosts has remained highly debated. Teleosts are thought to have evolved a unique mode of neurulation, whereby the neural plate infolds in absence of hingepoints and neural folds, at least in the hindbrain/trunk where it has been studied. Using high-resolution imaging and time-lapse microscopy, we show here the presence of these morphological landmarks in the zebrafish anterior neural plate. These results reveal similarities between neurulation in teleosts and other vertebrates and hence the suitability of zebrafish to understand human neurulation.

scholarly journals A gene regulatory network that underlies the derivation of the anterior neural plate from the epiblast

2010 ◽  
Vol 344 (1) ◽  
pp. 495
Author(s):  
Makiko Iwafuchi-Doi ◽  
Tatsuya Takemoto ◽  
Yuzo Yoshida ◽  
Isao Matsuo ◽  
Jun Aruga ◽  
...  
Keyword(s):  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Neural Plate ◽  
Gene Regulatory ◽  
Anterior Neural Plate

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.

scholarly journals Experiments on the Development of the Head of the Chick Embryo

1936 ◽  
Vol 13 (2) ◽  
pp. 219-236
Author(s):  
C. H. WADDINGTON ◽  
A. COHEN
Keyword(s):  
Thin Sheet ◽  
Neural Tissue ◽  
Primitive Streak ◽  
Neural Plate ◽  
Head Region ◽  
Process Stage ◽  
Optic Vesicles ◽  
Lens Formation ◽  
Embryonic Ectoderm

1. Experiments were made on the development of the head of chicken embryos cultivated in vitro. 2. Defects in the presumptive head region of primitive streak embryos are regulated completely if the wound fills up before the histogenesis of neural tissue begins in the head-process stage. Different methods by which the hole is filled are described. 3. No repair occurs in the head-process and head-fold stages, and in this period two masses of neural tissue cannot heal together. 4. Median defects, even if repaired as regards neural tissue, cause a failure of the ventral closure of the foregut. The lateral evaginations of the gut develop typically in atypical situations. The headfold may break through and join up with the endoderm in such a way that the gut acquires an anterior opening. 5. The paired heart rudiments may develop separately. The separate vesicles begin to contract at a time appropriate to the development of the embryo as a whole. The two hearts are mirror images, the left one having the normal curvature, but the embryos do not survive long enough for the hearts to acquire a very definite shape. 6. The forebrain has a considerable capacity for repair in the early somite stages (five to twenty-five somites). One-half of the forebrain can remodel itself into a complete forebrain. In some cases the neural plate and epidermis grow together over the wound, in others the epidermis and mesenchyme make the first covering, leaving a space along the inside of which the neural tissue grows. The neural tissue may become a very thin sheet. 7. The repaired forebrain may induce the formation of a nasal placode from the non-presumptive nasal epidermis which covers the wound. 8. If the optic vesicle is entirely removed, a new one is not formed, but parts of the vesicle can regulate to complete eye-cups, either when still attached to the forebrain or after being isolated in the extra-embryonic regions of another embryo. 9. Injured optic vesicles induce lenses from the non-presumptive epidermis which grows over the wound. Transplanted optic neural tissue from embryos of about five somites induces the formation of lentoids from extra-embryonic ectoderm, but only in a small proportion of cases. 10. The presumptive lens epidermis can produce a slight thickening even when contact with the optic cup is prevented. 11. The significance of periods of minimum regulatory power for the concept of determination is discussed. 12. The data concerning lens formation are discussed in terms of the field concept.

Inductive interactions direct early regionalization of the mouse forebrain

Development ◽  
1997 ◽  
Vol 124 (14) ◽  
pp. 2709-2718 ◽  
Author(s):  
K. Shimamura ◽  
J.L. Rubenstein
Keyword(s):  
Sonic Hedgehog ◽  
Bone Morphogenetic Proteins ◽  
Molecular Mechanisms ◽  
Neural Plate ◽  
Gene Encoding ◽  
Prechordal Plate ◽  
Optic Vesicles ◽  
The Central Nervous System ◽  
Anterior Neural Plate ◽  
Anterior Posterior

The cellular and molecular mechanisms that regulate regional specification of the forebrain are largely unknown. We studied the expression of transcription factors in neural plate explants to identify tissues, and the molecules produced by these tissues, that regulate medial-lateral and local patterning of the prosencephalic neural plate. Molecular properties of the medial neural plate are regulated by the prechordal plate perhaps through the action of Sonic Hedgehog. By contrast, gene expression in the lateral neural plate is regulated by non-neural ectoderm and bone morphogenetic proteins. This suggests that the forebrain employs the same medial-lateral (ventral-dorsal) patterning mechanisms present in the rest of the central nervous system. We have also found that the anterior neural ridge regulates patterning of the anterior neural plate, perhaps through a mechanism that is distinct from those that regulate general medial-lateral patterning. The anterior neural ridge is essential for expression of BF1, a gene encoding a transcription factor required for regionalization and growth of the telencephalic and optic vesicles. In addition, the anterior neural ridge expresses Fgf8, and recombinant FGF8 protein is capable of inducing BF1, suggesting that FGF8 regulates the development of anterolateral neural plate derivatives. Furthermore, we provide evidence that the neural plate is subdivided into distinct anterior-posterior domains that have different responses to the inductive signals from the prechordal plate, Sonic Hedgehog, the anterior neural ridge and FGF8. In sum, these results suggest that regionalization of the forebrain primordia is established by several distinct patterning mechanisms: (1) anterior-posterior patterning creates transverse zones with differential competence within the neural plate, (2) patterning along the medial-lateral axis generates longitudinally aligned domains and (3) local inductive interactions, such as a signal(s) from the anterior neural ridge, further define the regional organization.

Differential expression of multiple fork head related genes during gastrulation and axial pattern formation in the mouse embryo

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 47-59 ◽  
Author(s):  
H. Sasaki ◽  
B.L. Hogan
Keyword(s):  
Neural Crest ◽  
Floor Plate ◽  
Definitive Endoderm ◽  
Axis Formation ◽  
Adult Liver ◽  
Temporal And Spatial Patterns ◽  
Fork Head ◽  
Genes Encoding ◽  
Temporal And Spatial

Four genes encoding fork-head-domain-containing proteins (FD genes) have been isolated from a mouse 8.5 days post coitum (p.c.) embryo cDNA library. Two are mouse homologues of rat HNF-3 beta and HNF-3 alpha. The other two are novel and have been named MF-1 and MF-2 (for mesoderm/mesenchyme fork head). Wholemount in situ hybridization of embryos between 6.5 and 9.5 days p. c. shows that each gene has a unique expression pattern. HNF-3 beta is expressed in the node, notochord, floor plate and gut, while HNF-3 alpha is mainly in the definitive endoderm and gut, but also in the floor plate of the midbrain. These results suggest that HNF-3 beta and HNF-3 alpha, in addition to their known functions as transcriptional activators in adult liver, play a role in body axis formation, neural tube patterning and definitive endoderm formation during gastrulation. MF-1 RNA is present in non-notochordal mesoderm, and in neural-crest-derived head mesenchyme, while MF-2 transcripts are found in the sclerotomes of the somites and in head mesenchyme, including that from neural crest. Studies on gastrulation stage embryos suggest that the early temporal and spatial patterns of HNF-3 beta, MF-1 and HNF-3 alpha correlate with populations of cells undergoing commitment to different developmental fates. A model is proposed linking FD gene expression with gastrulation events in the mouse.

Disturbing endoderm signaling to anterior neural plate of vertebrates by the teratogen cadmium

2004 ◽  
Vol 18 (5) ◽  
pp. 653-660 ◽  
Author(s):  
Estı́baliz L Fernandez ◽  
Camilla Svenson ◽  
Lennart Dencker ◽  
Anne-Lee Gustafson
Keyword(s):  
Neural Plate ◽  
Anterior Neural Plate
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