Julie Adams

Degree Type

Honors Capstone Project

Date of Submission

Spring 5-1-2008

Capstone Advisor

Craig Albertson

Honors Reader

Larry Wolf

Capstone Major


Capstone College

Arts and Science

Audio/Visual Component


Capstone Prize Winner


Won Capstone Funding


Honors Categories

Sciences and Engineering

Subject Categories



Fibroblast growth factors are a family of intercellular signaling molecules that participate in the normal growth of the craniofacial skeleton. Advances in molecular genetics have revealed that fibroblast growth factors are involved in the regulation of bone growth by maintaining a balance between the differentiation of osteoblasts and the proliferation of mesenchyme (Morriss-Kay and Wilkie, 2005). The focus of my research is fibroblast growth factor 20a because it seems to play a significant role in the normal development of the skull. At birth, the skull is made up of bony elements, that meet at fibrous membranes called sutures. Throughout development, those bony elements fuse together at different rates to form solid bone. Previous research has shown that zebrafish deficient in fgf20a, which are referred to as dob mutants, have abnormal suture patterning and exhibit several craniofacial defects that are similar in presentation to the defects seen in individuals with craniosynostosis (Albertson, unpublished data). Craniosynostosis is a birth defect that is caused by the premature closure of sutures and is characterized by an irregular craniofacial shape. Using whole mount in situ hybridization (WISH) methods and advanced microscopic imaging, I gained insights into the pathological mechanisms that lead to aberrant suture formation in humans. Our research results suggest that fgf20a directly affects suture and skull development. We have demonstrated this in two ways. Firstly, we showed that in the absence of fgf20a, zebrafish have abnormal suture patterning. Secondly, we showed that the fgf20a gene is normally expressed in the cranial sutures of wild-type zebrafish through WISH methods. Our results are important because this is the first instance where an fgf ligand is implicated in craniosynostosis. Furthermore, we have established a molecular foothold (via fgf20a) into skull and suture development, and we have established a model system for studying the developmental origins and mechanisms of craniosynostosis.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

Included in

Biology Commons



To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.