Líffræðifélag Íslands
Líffræðiráðstefnan 2015
Erindi/veggspjald / Talk/poster V63
Ehsan Pashay Ahi (1), Benjamin S. Walker (2), Christopher S. Lassiter (2), Zophonías O. Jónsson (1,3)
1.Institute of Life and Environmental Sciences, University of Iceland, Sturlugata 7, 101 Reykjavik, Iceland, 2. Biology Department, Roanoke College, Salem VA, USA, 3. Biomedical Center, University of Iceland, Vatnsmýrarvegur 16, 101 Reykjavik, Iceland.
Kynnir / Presenter: Ehsan Pashay Ahi
Tengiliður / Corresponding author: Ehsan Pashay Ahi (epa1@hi.is)
The vertebrate craniofacial skeleton is a structurally complicated apparatus representing remarkable morphological diversity within and across species. The development of these skeletal structures requires well-orchestrated tissue interactions controlled by distinct molecular signals. Disruption of normal function of these molecular signals has been associated with a wide range of craniofacial malformations. Estrogen is a steroid molecule mediating a signaling cascade involved in a variety of developmental and physiological processes. Estrogen signaling also plays role in the formation of bone and cartilage, including craniofacial skeletogenesis. Studies in zebrafish have shown that while high concentrations of 17-β estradiol (E2) cause severe craniofacial defects, treatment with lower concentrations result in subtle changes in head morphology characterized by a shorter snout and flatter face. The molecular basis for these subtle morphological changes remains unexplored. In the present study we assess the effects of low E2 concentrations on the expression dynamics of sets of candidate genes during zebrafish larval head development. Using quantitative real-time PCR, we identified components of several pathways linked with skeletogenesis to be affected by treatment with E2. We found E2 mediated differential expression of genes involved in extracellular matrix (ECM) remodelling and skeletogenic pathways. Furthermore, we identified a co-expressed network of genes with a stronger inductive response to a lower dose of E2 during larval head development.