Valerie Horsley Gets Under Skin

The Yale University cell and molecular biologist is probing the deep mysteries of epidermal cells.

By Kerry Grens | May 1, 2017

© JANE SHAUCK PHOTOGRAPHYValerie Horsley was surrounded by academics from a young age. Raised by a single mother who began her doctoral work in industrial engineering when Horsley was seven, she spent a lot of time with graduate students who served as her babysitters. When it came time for her to graduate from Furman University in South Carolina with a biology degree, Horsley knew she needed her own PhD to become a professor and stay in academia.

She opted for Emory University, where her lack of in-depth molecular biology background became apparent. Horsley’s undergraduate career had been wide-ranging but not marked by copious research experience. “I felt completely overwhelmed,” she says. “But I think it actually helped me, because I learned to think broadly before I started thinking about specifics.”

Horsley joined the lab of Grace Pavlath, where she explored the role of a transcription factor called NFATc2. Pavlath’s team had previously found that mice lacking NFATc2 had smaller muscles, but they didn’t know why. Horsley found that the protein was critical for cells called myoblasts to fuse and form mature, multinucleated muscle fiber cells.1 “It revealed a novel step in the myogenesis pathway,” says Horsley, who also showed that NFATc2 regulated the transcription of a cytokine, IL-4. “Nobody knew muscle made IL-4,” says Pavlath. “It’s considered a landmark paper.”

For her postdoc, Horsley wanted to move out of muscle and into a different tissue, so she joined the Rockefeller University lab of Elaine Fuchs and dove into skin. One of her projects started with another transcription factor, Blimp1. When she knocked out the gene that encoded Blimp1, mice got oily skin. It turned out that Blimp1 was regulating the size of the sebaceous gland.2

See “More Than Skin Deep,” a profile of Elaine Fuchs

In 2009, Horsley set up her own lab at Yale University. Among several lines of inquiry, including characterizing the stages of keratinocyte specification and understanding adhesions between these epidermal cells, she’s been collaborating with her husband, Yale’s Matthew Rodeheffer, on the role of adipocytes in hair growth. They found that in the skin, adipogenesis occurs in parallel with the growth of hair, and regresses when hair follicles die.3 Although she wasn’t sure at first whether she wanted to collaborate with her husband, the partnership yielded an entirely new appreciation for fat cells in hair growth. “No one had looked at it before,” says Horsley. “It’s pretty much what my lab has been working on since.”

Horsley earned tenure last year. Away from the bench, she has been a leader in her department, and beyond. Yale’s Thomas Pollard, who helped hire Horsley, says that shortly after Horsley joined the university she began expanding the regular junior faculty lunches to other biology departments. Then she reached out to chemistry and physics PIs; then to all of arts and sciences, and eventually to the medical school as well. “No one asked her to do this. She just recognized that it was a good idea,” says Pollard. “This is not an exceptional thing for her to do. She does this all the time.” 


  1. V. Horsley et al., “IL-4 acts as a myoblast recruitment factor during mammalian muscle growth,” Cell, 113:483-94, 2003. Cited 360 times
  2. V. Horsley et al., “Blimp1 defines a progenitor population that governs cellular input to the sebaceous gland,” Cell, 126:597-609, 2006. Cited 334 times
  3. E. Festa et al., “Adipocyte lineage cells contribute to the skin stem cell niche to drive hair cycling,” Cell, 146:761-71, 2011. Cited 214 times

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Avatar of: James V. Kohl

James V. Kohl

Posts: 532

May 12, 2017

See also: Brain on stress: How the social environment gets under the skin

The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.”

The failure to provide a neurobiological framework for understanding natural selection for energy-dependent codon optimality, which is the basis for the biological embedding of epigenetically-effected positive health, positive affect, self-efficacy and self-esteem via effects on reactive alleles in the genome, continues to link all pathology from the virus-driven degradation of messenger RNA to the negative supercoiling of DNA.

No one asked me to establish that framework for healthy longevity or pathology, but I did it anyway after I was told to start with gene activation in GnRH neuroscrectory neurons by Bruce McEwen.


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