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Digital archive of theses discussed at the University of Pisa

 

Thesis etd-03012014-144543


Thesis type
Tesi di dottorato di ricerca
Author
MARRAS, GIULIA
URN
etd-03012014-144543
Thesis title
The role of the serotonergic receptor 2B in the ocular morphogenesis
Academic discipline
BIO/06
Course of study
SCIENZE BIOLOGICHE E MOLECOLARI
Supervisors
tutor Nardi, Irma
tutor Ori, Michela
Keywords
  • 5-HT2B
  • Neural Crest Cell
  • ocular morphogenesis
  • POM
  • serotonin
Graduation session start date
18/03/2014
Availability
Full
Summary
Serotonin (5-HT) is a well-known neurotransmitter that influences a wide variety of central and peripheral functions in the adult organism. During the development 5-HT plays also an important role in morphogenesis by modulating processes such as gastrulation, craniofacial and bone patterning and the generation of the left-right asymmetry, as well as in neural development and plasticity.
In the network of extracellular signals that orchestrates craniofacial and eye morphogenesis, it has been demonstrated that serotonin (5-HT) may play a role both in mouse and Xenopus. Most of the biological actions of 5-HT are mediated by G-coupled receptors and among these the 5-HT2B receptor seems to be particularly important in embryonic development. In fact it is an important regulator of cardiac morphogenesis and in previous works it has been shown that signaling through 5-HT2B is also involved in eye and craniofacial morphogenesis in Xenopus embryos.
Interestingly, our research group showed that the 5-HT2B gene is expressed in periocular mesenchyme that represents a key signaling center required for a correct eye morphogenesis.
Using Xenopus laevis as a model system, by means of loss-of function approach I investigated the 5-HT2B role focusing on the behavior and fate of the neural crest cells-periocular mesenchyme component underline the role of 5-HT2B in ocular morphogenesis. The abrogation of the 5-HT2B function in embryos resulted in the altered expression pattern of key genes involved in a proper ocular morphogenesis that cause formation of defective eyes, characterized by the failure of the optic fissure closure.
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