[citation needed] A large portion of Struhl’s research centers around the common fruit fly, or Drosophila, and the developmental genetics surrounding this type of insect.
[6] This mechanism was thought to be the method of reading the local slope of tissue-wide gradients of Fz activity, and that through this, all of the cells come to point in one direction.
[7] This paper concluded that Decapentaplegic (Dpp, a BMP) and Wingless (Wg, a Wnt) act together through a common mechanism in order to control wing growth as a function of morphogen range.
This paper proposed that Epsin was essential for cell signaling because it “targets mono-ubiquitinated DSL proteins to an endocytic recycling compartment that they must enter to be converted into active ligands”.
[8] Additionally, he proposed that Epsin “may be required to target mono-ubiquitinated DSL proteins to a particular subclass of coated pits that have special properties essential for Notch activation”.
[11] A research article published by Struhl in the American Academy of Arts and Sciences journal looked at the relationship between epigenetic states and inheritance of cis-acting chromatin modifications.
[12] In further research looking into the controls of Drosophila wing size, Struhl explored the mechanisms that limit growth as a function of time.
In 2004, Struhl was involved in a controversy regarding research on Wnt signaling, which is a major pathway in human cancer and embryonic development.
A postdoc named Siu-Kwong Chan performed experiments that came to the conclusion that the beta-catenin or Armadillo could transduce Wnt signals without entering the nucleus.