Abstract
The interaction between stem cells and their niche is essential for sustaining stem cell identity, and in the Drosophila testis, this interaction is maintained by E-cadherin. Our earlier work demonstrated that cadmium (Cd), an environmental toxicant, disrupts germline stem cell (GSC) homeostasis in Drosophila males, although the underlying molecular mechanisms remained unclear. In this study, we aimed to elucidate the mechanism by which Cd alters GSC homeostasis, using Drosophila testis as an in vivo model. Our findings show that Cd induced reactive oxygen species downregulate E-cadherin expression through modulation of JAK/STAT signaling pathway, resulting in disrupted GSC homeostasis, characterized by diminished stem cell pool and premature differentiation. Notably, overexpression of superoxide dismutase in early-stage of germ cells restored JAK/STAT signaling and E-cadherin levels. Additionally, early germ cells targeted E-cadherin overexpression with genetic background of stat92E knockdown showed significant recovery from aberrant GSC homeostasis under Cd exposure. Together, these results are consistent with a Cd mediated effect in which E-cadherin stands as a pivotal factor in maintaining GSC homeostasis. This study highlights the utility of Drosophila as an alternative model to investigate the role of cell adhesion molecules (CAMs) in stem cell regulation under chemical stress and further extended understanding about mechanistic insights mediating Cd toxicity in Drosophila.
