A key feature of many adult stem cell lineages is that cells undergo a limited number of transit amplifying (TA) mitotic divisions before initiating terminal differentiation, thus allowing production of many differentiated progeny per stem cell division. The number of TA divisions must be tightly regulated: too few may lead to defective tissue regeneration, too many to abnormal growth and cancer. We are investigating the molecular mechanisms that regulate and mediate the critical switch from TA cell proliferation to differentiation using the powerful Drosophila male germline stem cell lineage as an in vivo model. Specifically I will test the hypothesis that the switch from proliferation to differentiation is regulated by the tumor suppressor homolog Mei-P26 and Bam-dependant translational control. Translational control involving Mei-P26 protein may define a tumor suppressor mechanism in stem cell lineages and will shed light into how cells differentiate and how cancer arises.