To figure out where the lost germline stem cells went and how they lost the battle for space, the team returned to the microscope. This time, they examined the cells for whether they contained integrin, a protein that helps cells stick to each other. They found that somatic stem cells from flies lacking SOCS seemed to contain more integrin than somatic stem cells from flies with functional SOCS. According to Matunis, it's the increase in integrin that allows somatic stem cells to gain the upper hand because they can stick to the niche better than neighboring germline stem cells can.
Though the somatic stem cells were invading the niche, germline stem cells were not dying. In the microscope images, the team found that all remaining germline stem cells still looked alive and healthy, but elbowed out of their niche by somatic stem cells. Says Matunis, no matter how healthy a germline stem cell is, if it cannot stick, it will eventually be outcompeted by the somatic cells and pushed all the way out of the niche. Issigonis found the discovery remarkable: "The germline stem cells are perfectly fine," she says. "They're just leaving the niche and differentiating."
The team believes this model can be applied to other stem cell niches such as cancer. Just like the somatic stem cells overrunning the fly testes, cancer stem cells in mammalian systems become a danger when they become the stickiest cell in the niche. In both cases, the important control protein, SOCS, is lost. Knowing what is necessary for some stem cells to thrive and others to dwindle could have great importance to understanding the roots of stem cell diseases.
|Contact: Audrey Huang|
Johns Hopkins Medical Institutions