1: Dev Biol. 2004 Jul 15;271(2):439-66. 

Molecular anatomy of placode development in Xenopus laevis.

Schlosser G, Ahrens K.

Brain Research Institute, University of Bremen, 28334 Bremen, Germany.
gschloss@uni-bremen.de

We analyzed the spatiotemporal pattern of expression of 15 transcription factors
(Six1, Six4, Eya1, Sox3, Sox2, Pax6, Pax3, Pax2, Pax8, Dlx3, Msx1, FoxI1c, Tbx2,
Tbx3, Xiro1) during placode development in Xenopus laevis from neural plate to
late tail bud stages. Out of all genes investigated, only the expression of
Eya1, Six1, and Six4 is maintained in all types of placode (except the lens)
throughout embryonic development, suggesting that they may promote generic
placodal properties and that their crescent-shaped expression domain surrounding
the neural plate defines a panplacodal primordium from which all types of
placode originate. Double-labeling procedures were employed to reveal the
precise position of this panplacodal primordium relative to neural plate, neural
crest, and other placodal markers. Already at neural plate stages, the
panplacodal primordium is subdivided into several subregions defined by
particular combinations of transcription factors allowing us to identify the
approximate regions of origin of various types of placode. Whereas some types of
placode were already prefigured by molecularly distinct areas at neural plate
stages, the epibranchial, otic, and lateral line placodes arise from a common
posterior placodal area (characterized by Pax8 and Pax2 expression) and acquire
differential molecular signatures only after neural tube closure. Our findings
argue for a multistep mechanism of placode induction, support a combinatorial
model of placode specification, and suggest that different placodes evolved from
a common placodal primordium by successive recruitment of new inducers and
target genes.

PMID: 15223346 [PubMed - indexed for MEDLINE]


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2: Dev Biol. 2002 Sep 15;249(2):237-54. 

Extensive cell movements accompany formation of the otic placode.

Streit A.

Department of Craniofacial Development, King's College, Guy's Hospital, London
SE1 9RT, United Kingdom. andrea.streit@kcl.ac.uk

During development, the vertebrate inner ear arises from the otic placode, a
thickened portion of the ectoderm next to the hindbrain. Here, the first
detailed fate maps of this region in the chick embryo are presented. At head
process stages, placode precursors are scattered throughout a large region of
the embryonic ectoderm, where they intermingle with future neural, neural crest,
epidermal, and other placode cells. Within the next few hours, dramatic cell
movements shift the future otic placode cells toward the midline and ultimately
result in convergence to their final position next to rhombomeres 5-6.
Individual cells and small cell groups undergo constant cell rearrangements and
appear to sort out from nonotic cells. While the major portion of the otic
placode is derived from the nonneural ectoderm, the neural folds also contribute
cells to the placode at least until the four-somite stage. Comparison of these
fate maps with gene expression patterns at equivalent stages reveals molecular
heterogeneity of otic precursor cells in terms of their expression of dlx5,
msx1, Six4, and ERNI. Although Pax2 expression coincides with the region where
otic precursors are found from stage 8, not all Pax2-positive cells will
ultimately contribute to the otic placode.

PMID: 12221004 [PubMed - indexed for MEDLINE]


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3: Dev Genet. 1996;18(3):181-97. 

Genetic aspects of embryonic eye development in vertebrates.

Graw J.

Institut fur Saugetiergenetik, GSF-Forschungszentrum fur Umwelt und Gesundheit
Neuherberg, Oberschleissheim, Germany.

The vertebrate eye comprises tissues from different embryonic origins, e.g.,
iris and ciliary body are derived from the wall of the diencephalon via optic
vesicle and optic cup. Lens and cornea, on the other hand, come from the
overlying surface ectoderm. The timely action of transcription factors and
inductive signals ensure the correct development of the different eye
components. Establishing the genetic basis of eye defects has been an important
tool for the detailed analysis of this complex process. One of the main control
genes for eye development was discovered by the analysis of the allelic series
of the Small eye mouse mutants and characterized as Pax6. It is involved in the
interaction between the optic cup and the overlaying ectoderm. The central role
for Pax6 in eye development is conserved throughout the animal kingdom as the
murine Pax6 gene induces ectopic eyes in transgenic Drosophila despite the
obvious diverse organization of the eye in the fruit fly compared to
vertebrates. In human, mutations in the PAX6 gene are responsible for aniridia
and Peter's anomaly. In addition to Pax6, other mutations affecting the
interaction of the optic cup and the lens placode have been documented in the
mouse. For the differentiation of the retina from the optic cup several genes
are responsible: Mi leads to microphthalmia, if mutated, and encodes for a
transcription factor, which is expressed in the melanocytes of the pigmented
layer of the retina. In addition, further genes are implicated in the correct
development of the retina, e.g., Chx10, Dlx1, GH6, Msx1 and -2, Otx1 and -2, or
Wnt7b. Mutations within the retinoblastoma gene (RB1) are responsible for
retinal tumors. Knock-out mutants of RB1 exhibit a block of lens differentiation
prior to the retinal defect. Besides the influence of Rb1, the lens
differentiates under the influence of growth factors (e.g., FGF, IGF, PDGF,
TGF), and specific genes become activated encoding cytoskeletal proteins (e.g.,
filensin, phakinin, vimentin), structural proteins (e.g., crystallins) or
membrane proteins (e.g., Mip). The optic nerve originates from the neural
retina; ganglion cells grow to the optic stalk, forming the optic nerve. Its
retrograde walk to the brain through the rudiment of the optic stalk depends on
the correct Pax2 expression.

Publication Types:
    Review

PMID: 8631154 [PubMed - indexed for MEDLINE]


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