View Program - 63rd Annual Drosophila Research Conference

Adult stem cells become depleted throughout the lifetime of an organism, necessitating regenerative mechanisms to maintain the stem cell niche. Interestingly, signals for plastic regeneration mechanisms are often shared with those initiating tumorigenesis. A common feature of both plasticity and tumorigenesis is a reversion of differentiating cells to a stem-like state. The Drosophila male testis provides an invaluable model to study the process whereby differentiating cells transform into overproliferative tumor cells due to its distinct location and genetic tractability. Within the testis, the stem cell niche maintains both germline stem cells (GSCs) and somatic cyst stem cells (CySCs). GSCs divide asymmetrically to produce a differentiating daughter, which must become encapsulated, or encysted, by two CySC daughters. Our lab has developed a model whereby the coordinated release of this 2:1 soma-germline grouping is achieved via a modified cytokinesis program that pauses completion of GSC cytokinesis until somatic encystment of the germline is achieved. Whether this modified cytokinesis program becomes re-engaged during tumorigenesis and to what degree tumorous germ cells reinstate stem cell specific processes has yet to be explored. By genetically inducing tumorigenesis through ectopic expression of niche signals, we have visualized actin misregulation at the intercellular bridge and subsequent tumor fractionation by single cell abscission. We now aim to directly examine if tumor progression requires re-initiation of the stem cell-specific cytokinesis program. Examination of in vivo tumor proliferation will provide critical insights into the cell biology underlying tumorigenesis and may be useful in elucidating novel therapeutics for treatment of carcinoma.

Investigating re-initiation of stem cell cytokinesis during tumor proliferation