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Philip Reno

Philip Reno

Assistant Professor of Anthropology

512 Carpenter Building
Office Phone: (814) 863-7740

Curriculum Vitae

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  1. Ph.D. Biomedical Sciences, Kent State University
  2. MA Anthropology, Kent State University
  3. BA Anthropology, Washington University in St. Louis


Research Interests:

Hominid, primate and vertebrate evolutionary-developmental biology; evolution of primary and secondary sexual characters; skeletal biology; the developmental basis for morphological variation.

Ossification of the metacarpals  in an embryonic alligator.I study comparative primate and vertebrate evolution, with the primary goal to discover the genetic and developmental mechanisms that make us human. My lab is currently working on two main projects. The first is the role the regulation of the Androgen Receptor gene expression has in the evolution of secondary sexual characteristics. The wide diversity in male secondary sexual adornments suggests that multiple tissue specific enhancers tightly regulate AR expression. I use a variety of comparative, bioinformatic, and transgenic mouse experiments to identify these enhancers and understand how they pattern particular suites of sexually dimorphic features in humans and primates. Specifically we have identified a highly conserved mammalian enhancer adjacent to AR that drives gene expression in skin appendages, including sensory whiskers and penile spines. This enhancer has been lost in the human lineage since our divergence from chimpanzees and thus may be linked to the loss of penile spines and sensory whiskers in humans. Currently, my lab is working on recreating this deletion in mice, identifying other tissue specific enhancers surrounding the AR genes, and determining the role AR has in the formation of skin appendages such as penile spines.

Expression driven by a mouse Androgen Receptor enhancer (blue staining) in embryonic vibrissae, (arrows) hair follicles,and genital tubercle (upper right), as well as postnatal penile spines (lower right). The embryonic genital tubercle is a normal site of Androgen Receptor expression as shown by in situ hybridization (middle right)In addition, my lab also studies skeletal development and the particular cellular and genetic mechanisms underlying differential growth. In particular how do certain regions of the skeleton form growth plates while others do not, and why do these regions vary between species? To address this question we are using the natural variation in growth plate formation in the mammalian metatarsal.  As this bone forms only a single growth plate, we can compare the cellular behaviors, such as proliferation and gene expression, of the growth plate forming and non-forming ends.

Courses Taught:

  • Evolution and Development of Human Origins
  • Evolution of Human Walking

Recent Publications:

  • Reno PL, Lovejoy CO. (2015) From Lucy to Kadanuumuu: Balanced analyses of Australopithecus afarensis assembalges confirm only moderate skeletal dimorphism. PeerJ. 3:e925; DOI 10.7717/peerj.925.
  • Reno PL. (2014) Genetic and developmental basis for parallel evolution and its significance for understanding hominoid evolution. Evolutionary Anthropology. 23:188-200.
  • Kjosness KM, Hines JE, Lovejoy CO, Reno PL. (2014) The pisiform growth plate is lost in humans and supports a role for Hox in growth plate formation. Journal of Anatomy. 255:527-38.
  • Reno PL, McLean CY, Hines JE, Capellini TD, Bejerano G, Kingsley DM. (2013) A penile spine/vibrissa enhancer sequence is missing in modern and extinct humans, but is retained in multiple primates with sensory vibrissae and penile spines. PLoS ONE. 8(12): e84258. doi:10.1371/journal.pone.0084258
  • Reno PL, Horton WE, Lovejoy CO. (2013) Metapodial or phalanx? An evolutionary and developmental perspective on the homology of the first ray’s proximal segment. Journal of Experimental Zoology Part B. 320B:276-85.
  • McLean CY*, Reno PL*, Pollen AA*, Bassan AI, Capellini TD, Guenther C, Indjeian VB, Lim X, Menke DB, Schaar BT, Wenger AM, Bejerano G, and Kingsley DB. (2011) Human-specific loss of regulatory DNA and the evolution of human-specific traits. Nature. 471:216-19. * Equal author contribution