PUBLICATION
Zebrafish as a vertebrate model to study retinoic acid signalling in head mesoderm and pectoral fin development and to investigate non-ion channel epilepsies
- Authors
- Gibert, Y.
- ID
- ZDB-PUB-090603-36
- Date
- 2004
- Source
- Thesis : (Thesis)
- Registered Authors
- Gibert, Yann
- Keywords
- none
- MeSH Terms
- none
- PubMed
- none
Citation
Gibert, Y. (2004) Zebrafish as a vertebrate model to study retinoic acid signalling in head mesoderm and pectoral fin development and to investigate non-ion channel epilepsies. Thesis. .
Abstract
Retinoic acid (RA) is a key signal involved in the posteriorization of vertebrate neural ectoderm. The major enzyme involved in biosynthesis of RA during embryonic development is retinaldehyde dehydrogenase 2 (Raldh2). A zebrafish mutant in raldh2 (neckless; nls), which is devoid of RA signalling during embryonic development, exhibits anterior-posterior (AP) patterning defects in the neural ectoderm. Using the nls mutant I found that loss of RA also affects AP patterning of the cranial mesoderm. I depleted RA signalling in embryos and found that markers of the posterior cranial mesoderm are shortened along the AP axis, correlating with the severity of RA depletion. I determined the timing for requirement of RA to establish the AP-level of the posterior border of head mesoderm. Together with the pattern of raldh2 expression, I conclude that during gastrulation, RA biosynthesis in prospective mesoderm is a key signal for the specification of the AP extent of the posterior cranial mesoderm. RA-antagonist experiments further reveal that AP-patterning processes are coordinated between the neural tube and the paraxial mesoderm, aligning the hindbrain-spinal cord and head-trunk mesoderm boundaries.
Errata / Notes
Thesis, Konstanz University
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping