Cell-cell fusion is widely observed during development and disease and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing and delimited the event to the vicinity of the wound in the Drosophila larval epidermis. In the absence of JAK/STAT signaling, a large syncytium containing 3-fold the number of nuclei observed in wild-type tissue formed in wounded epidermis. upd2 and upd3 were transcriptionally induced by wounding and were required for suppressing excess cell fusion. JNK was activated in the wound vicinity and activity peaked at approximately 8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/STAT signaling was both necessary and sufficient for the induction of βPS integrin expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.
- Received February 10, 2016.
- Accepted April 18, 2017.
- © 2017. Published by The Company of Biologists Ltd