Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486759
Title: The role of eya1 and six1 during zebrafish otic development
Author: Blanco-Sanchez, Bernardo
Awarding Body: University of Sheffield
Current Institution: University of Sheffield
Date of Award: 2008
Availability of Full Text:
Access from EThOS:
Abstract:
In multicellular organisms, the differentiation program of a group of cells can be conceived of as a sequence· of developmental processes including induction, cell fate acquisition, patterning, cell death and morphogenetic movements. These processes are inter-dependent and need to be coordinated during embryogenesis. Eya and Six genes code for transcription factors that act together in a transcriptional complex. Both factors are required for the differentiation of distinct embryqnic structures such as the kidneys, pituitary gland and inner ear; in humans, mutations in EYAl or SIXl can cause Branchio-ato-Renal syndrome, characterised by otic, branchial arch and kidney defects. In the zebrafish, at 24 hpf, eyal and sixl are expressed in ventral otic epithelium, and interestingly the dog-eared/ eyar j- zebrafish mutant shows a characteristic misshapen ear at this stage: an elongated ·otic vesicle with a thicker dorsal epithelium in comparison to the wildtype. This observation suggests that eyal plays a role during the first !4 hours of otic development. Our results suggest that Eya! is not required for otic induction, and that, functions independently of previously characterised otic induction pathways. Instead, Eya! is required for acquisition of a correct morphology and for refinement of patterning within the otic vesicle as revealed by the expression of tbxl, otxl, pax2a, and snai/2. Eya! also plays a role in the neurogenic program giving rise to the statoacoustic ganglion. We showed that eyal function has a noncell autonomous effect in the regulation of tbxl otic expression. sixl zebrafish morphants phenocopy some of these aspects, such as the dorsal thickening of the otic vesicle at 24hpf, and the mispatterning of certain regions of the otic epithelium, but they also show some additional defects such as a somite phenotype. Nevertheless, six1 morphant otic phenotype is not identical to that of dogeared/ eyal mutant. The data from genetic interactions suggests that eyal genetically acts parallel to six1.
Supervisor: Not available Sponsor: Not available
Qualification Name: University of Sheffield, 2008 Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.486759  DOI: Not available
Share: