UNLABELLED: Cytoplasmic poly(A) tail length is a key regulator of mRNA translation and stability, controlled in part by non-canonical poly(A) polymerases of the TENT5 family, which are required for gametogenesis in mice. We characterize the sole Drosophila melanogaster TENT5 ortholog, which we name in step ( isep). Although identified as a candidate target of the eye-specification factor Eyeless, isep mutants have normal eyes; instead, isep is essential for male fertility. The isep gene and its protein are expressed in spermatocytes and in elongating spermatids and are concentrated at the distal end of spermatid cysts. Mutant spermatids fail to elongate normally and to individualize. Whole-testis poly(A) tail sequencing revealed that, unexpectedly for the loss of a poly(A) polymerase, median tail length increased in mutants, with lengthened transcripts enriched for roles in axoneme assembly. Both wild-type and a predicted catalytically inactive Isep rescued sterility. We propose that Isep controls localized translation of axonemal transcripts at the spermatid tip, largely independently of its poly(A) polymerase activity. ARTICLE SUMMARY: This work contributes to the Drosophila spermatogenesis community by identifying a previously unknown factor, isep, the fly's only TENT5, which makes flies a model to study this enzyme family. This work traces the expression pattern of both isep's transcripts and protein. Loss-of-function alleles generated by CRISPR-Cas9 mutagenesis result in complete male sterility, and immunofluorescence shows defects in spermatid elongation and individualization (separation into individual sperm). Mutant testes have longer median poly(A) tails, and lengthened transcripts are enriched for spermatogenesis and axonemal (sperm tail) genes. This work also suggests that the predicted poly(A) polymerase activity may be dispensable for spermatogenesis.