Anthony Mahowald

[3] At Johns Hopkins, Mahowald studied the structure of pole cells and polar granules in Drosophila melanogaster.

[3][5] Finally, from 1990 to 2002, Mahowald was employed at the University of Chicago as the department chair for molecular genetics and cellular biology.

In Drosophila testicles, the Leukocyte-antigen-related (LAR) receptor tyrosine phosphatase targets selection and synapse formation with nerve cells.

[8] After analysis of this data and further testing of his own, Mahowald discovered that the LAR expressed in the testicles retains germline stem cells at the niche through the increased E-cadherin-based adhesion.

[9] This creates very large cells, but their genetic information cannot be organized and separated into chromosomes due to inhibition of cyclin-dependent kinase activity.

[10] While organisms would die from the accumulation of aneuploid, Mahowald found that, in this instance, significant changes in survival rates were not observed.

Mahowald was concerned as to why organisms have multiple, very similar, genes that encode for the same proteins with only a few amino acids different.

[12] By using the Drosophila as an easily controlled genetic system, Mahowald and his team discovered that mutations in the Act5C gene caused organism death, indicating that Act5C did have an important and isolated function.

[12] However, a hybrid gene containing Act42A prevented organism death, indicating that the amino acid differences between the two isoforms are not significant.