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Credit: Andre Karwath
Experiments conducted in fruit flies showed that when researchers eliminated a type of stem cell, a group of non-stem cells stepped in to replace them.
The team said this discovery sheds new light on stem cell niches and may help explain how cancer stem cells (CSCs) replenish themselves after exposure to radiation and chemotherapy.
Erika Matunis, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and her colleagues detailed these findings in Cell Reports.
The researchers used the fruit fly as a model to examine stem cells in their natural state, studying stem cell niches in Drosophila testes.
In these niches are 3 kinds of cells: germ-line stem cells, which divide to produce sperm; somatic cyst stem cells, which make cyst cells; and hub cells, which produce signals that keep these 2 cell types going.
The hub cells have settled on their final form and are incapable of dividing further or changing their function—or so everyone thought.
In a bid to determine what happens when the somatic cyst stem cells are killed off, the researchers tried to figure out how to best do away with them. They thought the task would be straightforward, but it took many combinations of different genes working together to kill the somatic cyst cells.
“When we finally figured out a way to kill all of the somatic stem cells, we thought that the rest of the tissue would probably just empty out,” Dr Matunis said.
In 35% of testes, that’s just what happened. But in the rest, the somatic stem cells grew back.
This was a surprise, Dr Matunis said, and it raised the question of where these new stem cells originated.
The answer was another surprise: the hub cells. When the somatic stem cells were destroyed, the hub cells ramped up their machinery for cell division.
The team did several experiments to confirm the hub cells were involved, including one in which they genetically marked the hub cells and saw the mark appear in the newly formed somatic stem cells—a clear sign that hub cells had divided to make new stem cells.
Dr Matunis noted, however, that the new stem cells created by the hub cells weren’t exactly the same as the old ones. Sometimes, the new cells made molecules that only hub cells normally make.
As the researchers looked closer, they realized the damaged and recovered testes were making new niches. Instead of just one pocket of stem cells, a damaged testis might have 2 or 3.
The researchers have not determined how the new niches are formed, but they speculate that the original niche gets bigger as the new cells divide, then splits. The group is now conducting more experiments aimed at explaining the basics of how niches work, according to Dr Matunis.
She said this research may be useful for understanding CSCs. Knowing how tumor niches support the continued growth and division of CSCs might one day offer new targets for controlling such growth. 
Credit: Andre Karwath
Experiments conducted in fruit flies showed that when researchers eliminated a type of stem cell, a group of non-stem cells stepped in to replace them.
The team said this discovery sheds new light on stem cell niches and may help explain how cancer stem cells (CSCs) replenish themselves after exposure to radiation and chemotherapy.
Erika Matunis, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and her colleagues detailed these findings in Cell Reports.
The researchers used the fruit fly as a model to examine stem cells in their natural state, studying stem cell niches in Drosophila testes.
In these niches are 3 kinds of cells: germ-line stem cells, which divide to produce sperm; somatic cyst stem cells, which make cyst cells; and hub cells, which produce signals that keep these 2 cell types going.
The hub cells have settled on their final form and are incapable of dividing further or changing their function—or so everyone thought.
In a bid to determine what happens when the somatic cyst stem cells are killed off, the researchers tried to figure out how to best do away with them. They thought the task would be straightforward, but it took many combinations of different genes working together to kill the somatic cyst cells.
“When we finally figured out a way to kill all of the somatic stem cells, we thought that the rest of the tissue would probably just empty out,” Dr Matunis said.
In 35% of testes, that’s just what happened. But in the rest, the somatic stem cells grew back.
This was a surprise, Dr Matunis said, and it raised the question of where these new stem cells originated.
The answer was another surprise: the hub cells. When the somatic stem cells were destroyed, the hub cells ramped up their machinery for cell division.
The team did several experiments to confirm the hub cells were involved, including one in which they genetically marked the hub cells and saw the mark appear in the newly formed somatic stem cells—a clear sign that hub cells had divided to make new stem cells.
Dr Matunis noted, however, that the new stem cells created by the hub cells weren’t exactly the same as the old ones. Sometimes, the new cells made molecules that only hub cells normally make.
As the researchers looked closer, they realized the damaged and recovered testes were making new niches. Instead of just one pocket of stem cells, a damaged testis might have 2 or 3.
The researchers have not determined how the new niches are formed, but they speculate that the original niche gets bigger as the new cells divide, then splits. The group is now conducting more experiments aimed at explaining the basics of how niches work, according to Dr Matunis.
She said this research may be useful for understanding CSCs. Knowing how tumor niches support the continued growth and division of CSCs might one day offer new targets for controlling such growth.
Credit: Andre Karwath
Experiments conducted in fruit flies showed that when researchers eliminated a type of stem cell, a group of non-stem cells stepped in to replace them.
The team said this discovery sheds new light on stem cell niches and may help explain how cancer stem cells (CSCs) replenish themselves after exposure to radiation and chemotherapy.
Erika Matunis, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and her colleagues detailed these findings in Cell Reports.
The researchers used the fruit fly as a model to examine stem cells in their natural state, studying stem cell niches in Drosophila testes.
In these niches are 3 kinds of cells: germ-line stem cells, which divide to produce sperm; somatic cyst stem cells, which make cyst cells; and hub cells, which produce signals that keep these 2 cell types going.
The hub cells have settled on their final form and are incapable of dividing further or changing their function—or so everyone thought.
In a bid to determine what happens when the somatic cyst stem cells are killed off, the researchers tried to figure out how to best do away with them. They thought the task would be straightforward, but it took many combinations of different genes working together to kill the somatic cyst cells.
“When we finally figured out a way to kill all of the somatic stem cells, we thought that the rest of the tissue would probably just empty out,” Dr Matunis said.
In 35% of testes, that’s just what happened. But in the rest, the somatic stem cells grew back.
This was a surprise, Dr Matunis said, and it raised the question of where these new stem cells originated.
The answer was another surprise: the hub cells. When the somatic stem cells were destroyed, the hub cells ramped up their machinery for cell division.
The team did several experiments to confirm the hub cells were involved, including one in which they genetically marked the hub cells and saw the mark appear in the newly formed somatic stem cells—a clear sign that hub cells had divided to make new stem cells.
Dr Matunis noted, however, that the new stem cells created by the hub cells weren’t exactly the same as the old ones. Sometimes, the new cells made molecules that only hub cells normally make.
As the researchers looked closer, they realized the damaged and recovered testes were making new niches. Instead of just one pocket of stem cells, a damaged testis might have 2 or 3.
The researchers have not determined how the new niches are formed, but they speculate that the original niche gets bigger as the new cells divide, then splits. The group is now conducting more experiments aimed at explaining the basics of how niches work, according to Dr Matunis.
She said this research may be useful for understanding CSCs. Knowing how tumor niches support the continued growth and division of CSCs might one day offer new targets for controlling such growth.