Lecturer in Biology
B.S. – University of California, Irvine
M.S. – University of Hawaii
Ph.D. – University of Hawaii
E-mail – email@example.com
Phone – 540-568-8911
Fax – 540-568-3333
Office – Bioscience 2016H
Courses: Human Physiology (BIO 270), Animal Physiology (BIO 370)
Research Interests: Craniofacial morphogenesis
I am not currently doing research at JMU. However, the focus of my dissertation research was the development of the mammalian midface and the molecular factors involved in heritable frontonasal dysplasia (FND). Orofacial clefts are the most common of all human birth defects, striking 1.2 infants per 1000 births. FND, a type of orofacial cleft, is characterized by a median facial cleft, resulting from incomplete merging of the medial nasal prominences. We used a mouse mutant called Br, which displays the typical midfacial cleft of FND. Previous work has identified the transcription factor Six2 as the candidate gene for the Br mutation. Very little is known of the physiological relevance Six2 expression has on craniofacial morphogenesis. The objective of my dissertation was to elucidate the role Six2 plays in craniofacial morphogenesis utilizing a mouse model with FND associated with a deficiency in Six2 expression in the midfacial mesenchyme.
Hynd TE, Buckley CL, Lozanoff S. 2013. Case of cephalothoracopagus conjoined twinning in an embryonic mouse. Birth Defects Res A Clin Mol Teratol. 97(6):421-424.
Somponpun SJ, Wong B, Hynd TE, Fogelgren B, Lozanoff S. 2011. Osmoregulatory defect in adult mice associated with deficient prenatal expression of six2. Am J Physiol Regul Integr Comp Physiol. 301(3):R682-689.