Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.

Profile Publications (8)
XB-PERS-2605
Name: Alexander M. Schreiber
Position: Assistant Professor
Research Description:
y research interests: 
Nothing fascinates me more in this world than the mystery of vertebrate metamorphosis. How does a tadpole turn into a frog? What genes mediate the abrupt transformation of a larval fish or amphibian into its juvenile form? How did metamorphosis evolve?

I study metamorphosis in two very different species: the African clawed frog, Xenopus laevis, and marine flatfishes (flounder, halibut, soles, tonguefish). Unlike frogs, which are typical bilaterally symmetrical vertebrates, adult flatfish are the most behaviorally lateralized and morphologically asymmetrical vertebrates the world has ever known: they have both eyes on the same side of the head, and they spend their lives swimming on one side. Interestingly, flatfish LARVAL morphology and behavior resembles that of other fish: their skull morphology is bilaterally symmetrical, and they swim with an upright posture. However, several weeks to months after hatching, these larval flatfish experience one of nature’s most dramatic transformations: first, they begin to develop a highly lateralized swimming posture similar to that of the adult, and second, their skull remodels abruptly, facilitating the migration of one eye over the top of the head to the other side.

The diverse developmental programs of tadpole metamorphosis, such as programmed cell death (e.g. gill and tail resorption), cell proliferation (limb growth), and organ remodeling (brain, skull, and gut) are mediated entirely by one small molecule: thyroid hormone (TH). In the absence of TH, a tadpole will grow, but will never turn into a frog. The receptors for TH are nuclear transcription factors that bind to specific regions of DNA (thyroid response elements, or TREs) located within the promoter regions of some genes; the binding of TH and its receptors to these TREs causes thyroid hormone responsive genes to be turned on or off to carry out different metamorphic programs. Incredibly, thyroid hormone appears to mediate this indirect development in ALL metamorphosing vertebrates, including flatfish.

My current projects: 
The use of transgenically-modified frogs to study tissue-tissue interactions and organ remodeling during frog metamorphosis

Lab Memberships

Schreiber Lab (Principal Investigator/Director)

Contact Information

Address:
St Lawerence University
23 Romoda Drive
Canton, NY
13617, USA


Web Page: http://www.stlawu.edu/news/bios/node/124