2,761 research outputs found
Coordinate actions of BMPs, Wnts, Shh and noggin mediate patterning of the dorsal somite
Shortly after their formation, somites of vertebrate embryos
differentiate along the dorsoventral axis into sclerotome,
myotome and dermomyotome. The dermomyotome is then
patterned along its mediolateral axis into medial, central
and lateral compartments, which contain progenitors of
epaxial muscle, dermis and hypaxial muscle, respectively.
Here, we used Wnt-11 as a molecular marker for the medial
compartment of dermomyotome (the āmedial lipā) to
demonstrate that BMP in the dorsal neural tube indirectly
induces formation of the medial lip by up-regulating Wnt-1
and Wnt-3a (but not Wnt-4) expression in the neural tube.
Noggin in the dorsal somite may inhibit the direct action of
BMP on this tissue. Wnt-11 induction is antagonized by
Sonic Hedgehog, secreted by the notochord and the floor
plate. Together, our results show that the coordinated
actions of the dorsal neural tube (via BMP and Wnts), the
ventral neural tube/notochord (via Shh) and the somite
itself (via noggin) mediates patterning of the dorsal compartment of the somite
Neural tube-ectoderm interactions are required for trigeminal placode formation
Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode
Competence, specification and induction of Pax-3 in the trigeminal placode
Placodes are discrete regions of thickened ectoderm that contribute extensively to the peripheral nervous system in the vertebrate head. The paired-domain transcription factor Pax-3 is an early molecular marker for the avian ophthalmic trigeminal (opV) placode, which forms sensory neurons in the ophthalmic lobe of the trigeminal ganglion. Here, we use collagen gel cultures and heterotopic quail-chick grafts to examine the competence, specification and induction of Pax-3 in the opV placode. At the 3-somite stage, the whole head ectoderm rostral to the first somite is competent to express Pax-3 when grafted to the opV placode region, though competence is rapidly lost thereafter in otic-level ectoderm. Pax-3 specification in presumptive opV placode ectoderm occurs by the 8-somite stage, concomitant with robust Pax-3 expression. From the 8-somite stage onwards, significant numbers of cells are committed to express Pax-3. The entire length of the neural tube has the ability to induce Pax-3 expression in competent head ectoderm and the inductive interaction is direct. We propose a detailed model for Pax-3 induction in the opV placode
Azobenzene versus 3,3',5,5'-tetra-tert-butyl-azobenzene (TBA) at Au(111): Characterizing the role of spacer groups
We present large-scale density-functional theory (DFT) calculations and
temperature programmed desorption measurements to characterize the structural,
energetic and vibrational properties of the functionalized molecular switch
3,3',5,5'-tetra-tert-butyl-azobenzene (TBA) adsorbed at Au(111). Particular
emphasis is placed on exploring the accuracy of the semi-empirical dispersion
correction approach to semi-local DFT (DFT-D) in accounting for the substantial
van der Waals component in the surface chemical bond. In line with previous
findings for benzene and pure azobenzene at coinage metal surfaces, DFT-D
significantly overbinds the molecule, but seems to yield an accurate adsorption
geometry as far as can be judged from the experimental data. Comparing the
trans adsorption geometry of TBA and azobenzene at Au(111) reveals a remarkable
insensitivity of the structural and vibrational properties of the -N=N- moiety.
This questions the established view of the role of the bulky tert-butyl-spacer
groups for the switching of TBA in terms of a mere geometric decoupling of the
photochemically active diazo-bridge from the gold substrate.Comment: 9 pages including 6 figures; related publications can be found at
http://www.fhi-berlin.mpg.de/th/th.htm
Rhombomere of origin determines autonomous versus environmentally regulated expression of Hoxa3 in the avian embryo
We have investigated the pattern and regulation of Hoxa3 expression in the hindbrain and associated neural crest cells in the chick embryo, using whole mount in situ hybridization in conjunction with DiI labeling of neural crest cells and microsurgical manipulations. Hoxa3 is expressed in the neural plate and later in the neural tube with a rostral border of expression corresponding to the boundary between rhombomeres (r) 4 and 5. Initial expression is diffuse and becomes sharp after boundary formation. Hoxa3 exhibits uniform expression within r5 after formation of rhombomeric borders. Cell marking experiments reveal that neural crest cells migrating caudally, but not rostrally, from r5 and caudally from r6 express Hoxa3 in normal embryo. Results from transposition experiments demonstrate that expression of Hoxa3 in r5 neural crest cells is not strictly cell-autonomous. When r5 is transposed with r4 by rostrocaudal rotation of the rhomobomeres, Hoxa3 is expressed in cells migrating lateral to transposed r5 and for a short time, in condensing ganglia, but not by neural crest within the second branchial arch. Since DiI-labeled cells from transposed r5 are present in the second arch, Hoxa3-expressing neural crest cells from r5 appear to down-regulate their Hoxa3 expression in their new environment. In contrast, when r6 is transposed to the position of r4 after boundary formation, Hoxa3 is maintained in both migrating neural crest cells and those positioned within the second branchial arch and associated ganglia. These results suggest that Hoxa3 expression is cell-autonomous in r6 and its associated neural crest. Our results suggest that neural crest cells expressing the same Hox gene are not eqivalent; they respond differently to environmental signals and exhibit distinct degrees of cell autonomy depending upon their rhombomere of origin
Dorsal hindbrain ablation results in rerouting of neural crest migration and changes in gene expression, but normal hyoid development
Our previous studies have shown that hindbrain neural
tube cells can regulate to form neural crest cells for a
limited time after neural fold removal (Scherson, T.,
Serbedzija, G., Fraser, S. E. and Bronner-Fraser, M. (1993).
Development 188, 1049-1061; Sechrist, J., Nieto, M. A.,
Zamanian, R. T. and Bronner-Fraser, M. (1995). Development
121, 4103-4115). In the present study, we ablated the
dorsal hindbrain at later stages to examine possible alterations in migratory behavior and/or gene expression in
neural crest populations rostral and caudal to the operated
region. The results were compared with those obtained by
misdirecting neural crest cells via rhombomere rotation.
Following surgical ablation of dorsal r5 and r6 prior to the
10 somite stage, r4 neural crest cells migrate along normal
pathways toward the second branchial arch. Similarly, r7
neural crest cells migrate primarily to the fourth branchial
arch. When analogous ablations are performed at the 10-
12 somite stage, however, a marked increase in the numbers
of DiI/Hoxa-3-positive cells from r7 are observed within the
third branchial arch. In addition, some DiI-labeled r4 cells
migrate into the depleted hindbrain region and the third
branchial arch. During their migration, a subset of these r4
cells up-regulate Hoxa-3, a transcript they do not normally
express. Krox20 transcript levels were augmented after
ablation in a population of neural crest cells migrating from r4, caudal r3 and rostral r3. Long-term survivors of
bilateral ablations possess normal neural crest-derived
cartilage of the hyoid complex, suggesting that misrouted
r4 and r7 cells contribute to cranial derivatives appropriate for their new location. In contrast, misdirecting of the neural crest by rostrocaudal rotation of r4 through r6 results in a reduction of Hoxa-3 expression in the third branchial arch and corresponding deficits in third arch-derived structures of the hyoid apparatus. These results demonstrate that neural crest/tube progenitors in the hindbrain can compensate by altering migratory trajectories and patterns of gene expression when the adjacent neural crest is removed, but fail to compensate appropriately when the existing neural crest is misrouted by neural tube rotation
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