This web page was produced as an assignment for Genetics 677, an undergraduate course at UW-Madison
Future Directions
There is still so much unknown about not only genderblind and its homologs but also about a biological basis for homosexuality. Money is scarce for research into what still remains a very controversial topic. If I could have all of the resources that I need I would look at these four problems that I came across while doing my research:
1) Determine what specifies genderblind (and its homologs) to glutamate. I showed previously that the protein domain in genderblind is found in many other proteins that are unrelated to both glutamate transport and mating behavior. I would focus my research on the small parts of the protein on either end of the Amino Acid Permease 2 domain since those are the parts that are not conserved across proteins.
2) Determine how the drop in extracellular glutamate concentration causes bi-sexual behavior. What about glutamate specifically causes this massive behavioral change. To do so I would look at the cells downstream of the glutamate pathway, the ones that receive the glutamate and see what the decrease in glutamate changes in its cellular functions.
3) Whether the same system applies to females and why or why not? The original genderblind paper (1) never addressed female genderblind mutants so I am interested in whether or not the same behaviors can be seen and if they cannot, then why?
4) Repeat the genderblind experiment in mice. I would knockout the mouse homolog of genderblind (SLC7A6) and see if the same bi-sexual behavior can be observed. If it is indeed observed, I would say that genderblind and all of its homologs could be considered viable candidates for being the "gay" gene since its function and phenotype would be conserved from flies to mammals.