such as "Introduction", "Conclusion"..etc
December 14, 2005 -- The lens in the developing eye acts as a TGFbeta signaling center that
controls differentiation, survival and formation of multiple eye
structures deriving from the neural crest. A study published today in
the open access journal Journal of Biology shows that neural crest (NC)
derived cells contribute to both anterior and posterior parts of the
developing mammalian eye. NC cells migrate properly in the eye but fail
to differentiate in the absence of TGFbeta signaling. The activity of
TGFbeta is mediated by the two transcription factors Foxc1 and Pitx2
that have been implicated in human eye disorders. These findings shed
light on the origin of congenital eye disorders that can give rise to
glaucoma and blindness: Axenfeld-Rieger's anomaly and persistent
hyperplastic primary vitreous.
Sommer, from the Institute of Cell Biology at the ETH in Zurich,
Switzerland, heading an international team including Lars Ittner, used
in vivo cell fate mapping in mice. They show that NC-derived cells can
be found in the eye vesicle of mouse embryos, soon after it is formed.
NC-derived cells subsequently contribute to various structures of the
developing eye, and Ittner et al. show for the first time an NC
contribution to the primary vitreous.
TGFbeta receptor type 2, Tgfbr2, was inactivated to study the
importance of the signaling pathway in NC-derived cells. In these mice,
the eyes were reduced in size and the lens and cornea failed to
separate. The authors show that TGFbeta signaling is crucial for proper
differentiation and morphogenesis of NC-derived cells in eye
structures. Conceivably, TGFbeta might be able to support
differentiation not only during eye development but also at later
stages. If so, this might open up new strategies for promoting
regeneration of eye structures, for example in patients suffering from
loss of corneal transparency.
Source : BioMed Central
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