User talk:Z3333865

From Embryology
Revision as of 16:32, 14 September 2012 by Z3333865 (talk | contribs)
time text
time text
time text
time text
time text
time text
time text
time text
time text
time text
time text
time text
time text

DRAFT - RANDOM INFORMATION

  • the production of auditory and vestibular neurons tends to occur in ventral and anterior regions of the ear and is preceded by the expression of proneural genes such as Ngn1 in the anteroventral otocyst (Raft et al., 2004).
  • The fixing of each axis occurs at different times, with anterior-posterior fates becoming permanent before dorsal-ventral fates (Wu et al., 1998) --> different signals involved.
  • inner ear has an obvious DV polarity, with the vestibular apparatus located dorsally and the sound-detecting cochlea emerging as a ventral protrusion of the otocyst
  • signals from the neural tube might specify the DV axis of the inner ear (Choo et al., 2006)
  • Shh produced by the notochord and floor plate acts as a morphogen to pattern the DV neural tube (Dessaud et al., 2008), and this diffusible signal also acts directly on the developing amniote otocyst to confer DV patterning (Riccomagno et al., 2002; Bok et al., 2007b; Whitfield and Hammond, 2007).
  • Receptors are expressed in a dorsal-to-ventral gradient, indicative of a graded response to Shh and signalling development of ventral inner ear structures
  • loss of ventral patterning information is translated into a loss or reduction of ventral structures, including the cochlea and cochleovestibular ganglion (Bok et al., 2005; Riccomagno et al., 2002).
  • repressing Hedgehog signalling is also needed to allow for normal development of dorsal and lateral structures of the inner ear (Hammond et al., 2010).
  • ventral inner ear (cochlea and saccule), dorsal inner ear (semicircular canal, endolymphatic duct, cristae and utricle)
  • as reviewed by <pubmed>22186725</pubmed> data suggests that Shh acts on the ventral otocyst directly to regulate cochlear development, and that dorsal development can be regulated by signals from tissues adjacent to the otocyst that require Shh signaling for their normal development.
  • ventralizing effects of Shh are complemented by dorsalizing signals, again located in the midline. Wnt reporter mice have revealed that the initial mediolateral gradient of Wnt signaling seen in the otic placode, which is likely to be due to Wnt8 in the hindbrain (Urness et al., 2010) or Wnt6 at the hindbrain/placode boundary (Jayasena et al., 2008), is preserved as a DV gradient as the placode invaginates and closes to form the otocyst (Ohyama et al., 2006; Riccomagno et al., 2005).
  • Evidence suggests that Wnt and Shh signals regulate different inner ear genes in different ways, with opposing gradients of Shh and Wnt signaling regulating the spatial localization of transcription factors, ultimately leading to the differentiation of a correctly patterned inner ear.