Drosophila genes that affect centrosome function were assessed for capacity to produce tumors in a larval brain system. Candidate mutations were characterized using a tissue transplant assay for neoplastic capacity in which larval brain tissue is transplanted into the abdomens of wild-type adult female hosts. For loss-of-function mutations in Sas-4, polo, and aurA, brain tissue transplants exhibited unrestrained growth, filling the abdominal cavity, and killing a subset of the hosts; small colonies scattered on different parts of the host's anatomy (micrometastases) are observed. The tumors can be maintained by serial retransplantation; these tumor lines exhibit increasing amounts of polyploidy and chromosome instability (CIN).
Based on two additional observations, it has been postulated that development of tumors in neural tissues due to centrosome dysfunction is caused primarily by perturbation of the self-renewing asymmetric division of neural stem cells, rather than by CIN. First, other sources of CIN (genetic or environmental) did not result in significant tumorigenic phenotypes in the larval brain transplantation assay. Second, when imaginal disc (epithelial) tissues from loss-of-function mutations in Sas-4, polo, and aurA were transplanted into the abdomens of wild-type adult female hosts, no tumorous growth was observed.
[updated May 2019 by FlyBase; FBrf0222196]