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Cells Take Sole Responsibility for Merkel Cell Maintenance

27.01.2015

Researchers have identified a population of “progenitor” cells in the skin that are solely responsible for the generation and maintenance of touch-sensing Merkel cells. The study appears in The Journal of Cell Biology.

Merkel cells are unique cells located in the epidermis, the outermost layer of the skin. Through connections to nerve endings, Merkel cells play critical roles in our sense of touch. They are hypothesized to be the cells that undergo cancerous transformation and cause Merkel cell carcinoma, an aggressive form of skin cancer with no effective treatment.


Wright et al., 2015

After six months, whisker follicles in adult mice lacking Atoh1-expressing progenitor skin cells (left) have a deficiency of Merkel cells (green) compared with a control group (right).

Merkel cells require a transcription factor called Atoh1 for their specification. But the identity of the progenitor, or stem cells, that give rise to Merkel cells during embryonic development and adulthood is unclear.

In the study, Stephen Maricich and colleagues identified a subpopulation of Atoh1-expressing cells in hair and whisker follicles within mouse skin that exclusively give rise to Merkel cells during development and adulthood. Removing Atoh1-positive skin cells in adult mice led to a permanent reduction in Merkel cell numbers, showing that other stem cell populations are incapable of producing Merkel cells.

Importantly, the findings suggest that, if Merkel cell carcinoma does arise from Merkel cell progenitors, then Atoh1-positive Merkel cell precursors could be the cells of origin. This discovery will therefore help researchers dissect the cell-specific events mediating tumorigenesis in the particular case of Merkel cell carcinoma.

Wright, M.C., et al. 2015. J. Cell Biol. doi:10.1083/jcb.201407101

About The Journal of Cell Biology
The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jcb.org

Research reported in the press release was supported by the National Institutes of Health and the Richard King Mellon Foundation Institute for Pediatric Research.

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