Control of Stem Cell Self-Renewal in <i>Drosophila</i> Spermatogenesis by JAK-STAT Signaling

TLDR

Stem cells regenerate tissue and maintain their population through self‑renewal, a process regulated by niche signals such as the hub‑derived Unpaired ligand that activates JAK‑STAT signaling in Drosophila testes. The study aims to molecularly characterize the niche that controls stem cell self‑renewal in Drosophila testes. Loss of JAK‑STAT signaling causes germ‑line stem cells to differentiate without self‑renewal, whereas ectopic activation expands both germ‑line and somatic stem cells, demonstrating that hub‑derived JAK‑STAT signaling defines the stem‑cell niche.

Abstract

Stem cells, which regenerate tissue by producing differentiating cells, also produce cells that renew the stem cell population. Signals from regulatory microenvironments (niches) are thought to cause stem cells to retain self-renewing potential. However, the molecular characterization of niches remains an important goal. In Drosophila testes, germ line and somatic stem cells attach to a cluster of support cells called the hub. The hub specifically expresses Unpaired, a ligand activating the JAK-STAT (Janus kinase-signal transducer and activator of transcription) signaling cascade. Without JAK-STAT signaling, germ line stem cells differentiate but do not self-renew. Conversely, ectopic JAK-STAT signaling greatly expands both stem cell populations. We conclude that the support cells of the hub signal to adjacent stem cells by activation of the JAK-STAT pathway, thereby defining a niche for stem cell self-renewal.