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Scientists identify gene involved in stem cell self-renewal in planarians
James E.
Kloeppel, Physical Sciences Editor
217-244-1073; kloeppel@uiuc.edu
8/7/06
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CHAMPAIGN, Ill. —
No matter how you slice it, the freshwater planarian possesses an amazing
ability to regenerate lost body parts. Chop one into pieces, and each
piece can grow into a complete planarian. The flatworm relies upon a
population of stem cells to accomplish this remarkable feat; recent
work sheds light on how planarians maintain these stem cells throughout
their lives.
In a paper to appear in the August issue of the journal Developmental
Cell, scientists show that a member of the Bruno-like family of RNA
binding proteins – produced by a gene found in both planarians
and humans – plays a vital role in maintaining the stem cell population
in the planarian Schmidtea mediterranea. The work could lead to a better
understanding of the fundamental mechanisms by which stem cells are
regulated; such basic understanding is required for the successful therapeutic
application of stem cells in humans.
“One of the defining characteristics of stem cells is their ability
to self-renew – that is, to make more stem cells in addition to
differentiating into multiple cell types,” said Phillip A. Newmark,
a professor of cell and developmental
biology at the University of Illinois at Urbana-Champaign and corresponding
author of the paper. “We found that in the absence of this protein,
the stem cells could respond to wound stimuli, proliferate, and differentiate,
but they were unable to self-renew. As a result, the regeneration process
failed and the animals died.”
Using a technique called RNA interference, Illinois graduate student
Tingxia Guo and Newmark first eliminated most of the Bruno-like protein
(Bruli) from a number of planarians. Then they amputated a small piece
from each flatworm.
In the usual manner, the planarian stem cells migrated to the site of
the wound, sensed what was missing and began rebuilding. Regeneration
ceased, however, when the stem cell population became depleted.
“Had Bruli protein been present, the regeneration process would
have continued to completion,” Newmark said. “What may be
happening is that when this protein is eliminated, RNAs that are supposed
to be turned off (that is, not made into proteins) are now turned on
and made into proteins. Those proteins may then cause the stem cells
to differentiate, instead of also producing new stem cells to maintain
the population.”
While there is still much to be learned about stem cell self-renewal,
the researchers’ results suggest that Bruli protein is required
for stem cell maintenance in planarians.
“The next steps are to see if the gene that makes this protein
in planarians plays a similar role in stem cells in other organisms
and to identify possible RNA targets of this protein,” Newmark
said.
In addition to Newmark and Guo, Antoine Peters at the Friedrich Miescher
Institute for Biomedical research in Basel, Switzerland, was a co-author
on the paper. Funding was provided by the National Institutes of Health,
the National Science Foundation, and the Damon Runyon Cancer Research
Foundation.
Editor’s note: To reach Phillip Newmark, call 217-244-4674; e-mail: pnewmark@uiuc.edu.
