Tubulin-binding cofactor E-like (TBCEL), the protein product of the <i>mulet</i> gene, is required in the germline for the regulation of inter-flagellar microtubule dynamics during spermatid individualization

Individual sperm cells are resolved from a syncytium during late step of spermiogenesis known as individualization, which is accomplished by an Individualization Complex (IC) composed of 64 investment cones. <i>mulet</i> encodes Tubulin-binding cofactor E-like (TBCEL), suggesting a role for microtubule dynamics in individualization. Indeed, a population of ∼100 cytoplasmic microtubules fails to disappear in <i>mulet</i> mutant testes during spermatogenesis. This persistence, detected using epi-fluorescence and electron microscopy, suggests that removal of these microtubules by TBCEL is a prerequisite for individualization. Immunofluorescence reveals TBCEL expression in elongated spermatid cysts. In addition, testes from <i>mulet</i> mutant males were rescued to wild type using <i>tubulin-Gal4</i> to drive TBCEL expression, indicating that the mutant phenotype is caused by the lack of TBCEL. Finally, RNAi driven by <i>bam</i>-GAL4 successfully phenocopied <i>mulet</i>, confirming that <i>mulet</i> is required in the germline for individualization. We propose a model in which the cytoplasmic microtubules serve as alternate tracks for investment cones in <i>mulet</i> mutant testes.This article has an associated First Person interview with the first author of the paper.