Fgf8 regulation of parasympathetic postganglionic neuron development

dc.contributor.advisorGaufo, Gary O.
dc.contributor.authorChen, Yi-Ju
dc.contributor.committeeMemberWilson, Charles J.
dc.contributor.committeeMemberMueller, Paul R.
dc.contributor.committeeMemberLundell, Martha J.
dc.contributor.committeeMemberVogel, Kristine S.
dc.date.accessioned2024-02-09T20:20:06Z
dc.date.available2024-02-09T20:20:06Z
dc.date.issued2011
dc.descriptionThis item is available only to currently enrolled UTSA students, faculty or staff. To download, navigate to Log In in the top right-hand corner of this screen, then select Log in with my UTSA ID.
dc.description.abstractThe cranial parasympathetic reflex circuit contains sensory, pre- and postganglionic neurons. How this circuit is wired and the cues that control this process are unknown. We discovered that the fate of neural crest (NC)-derived postganglionic (PG) neurons depends on interaction with complementary placode-derived sensory ganglia. We show that the expression of Fgf8 in the head is strategically poised to control this cellular relationship. Loss of Fgf8 globally leads to an early loss of placodal ganglia and reduced number of PG neurons. The latter finding is associated with the early loss of NC by apoptosis. This loss occurs concurrent with the interaction between the NC and placodal ganglia. Analyses of tissue-specific loss of Fgf8 show that Fgf8 regulates the differentiation of PG neurons by different mechanisms. For example, mesodermal Fgf8 deficiency leads to a loss in PG neurons that is independent of NC apoptosis or defects in placodal ganglia, but dependent on early differentiation of PG precursors. Ectodermal Fgf8 deficiency also causes a reduction of PG neurons. However, the mechanism occurs through regulating early proliferation and later differentiation of PG precursors. Loss of PG neurons is a consequence of Fgf8 from mesoderm and ectoderm binding to Fgf receptors on the NC, requiring both Fgfr1 and Fgfr2. Finally, we show that the interaction of NC and placodal cells is not hard-wired, but plastic along the anterior-posterior axis. Our findings provide a general principle by which the formation of the parasympathetic circuit depends on the interaction of its precursors and fgf8 signals.
dc.description.departmentIntegrative Biology
dc.format.extent141 pages
dc.format.mimetypeapplication/pdf
dc.identifier.isbn9781267084453
dc.identifier.urihttps://hdl.handle.net/20.500.12588/3195
dc.languageen
dc.subjectcranial neural crest
dc.subjectepibranchial placode
dc.subjectFgf8
dc.subjectFgfr1/Fgfr2
dc.subjectparasympathetic nervous system
dc.subjectpostganglionic neurons
dc.subject.classificationDevelopmental biology
dc.subject.classificationNeurosciences
dc.subject.classificationGenetics
dc.titleFgf8 regulation of parasympathetic postganglionic neuron development
dc.typeThesis
dc.type.dcmiText
dcterms.accessRightspq_closed
thesis.degree.departmentIntegrative Biology
thesis.degree.grantorUniversity of Texas at San Antonio
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy

Files

Original bundle

Now showing 1 - 1 of 1
No Thumbnail Available
Name:
Chen_utsa_1283D_10630.pdf
Size:
74.74 MB
Format:
Adobe Portable Document Format