Guillermo Oliver

Guillermo Oliver is a Uruguayan-American research scientist. He is currently the Thomas D. Spies Professor of Lymphatic Metabolism at Northwestern University, and director of the Center for Vascular and Developmental Biology at the Feinberg Cardiovascular Research Institute. Oliver is an elected member of both the American Association for the Advancement of Science and the Academia de Ciencias de América Latina.

Guillermo Oliver
Born1955
Montevideo, Uruguay
Alma materUniversity of Uruguay, National University of Mexico, and UCLA
OccupationProfessor
EmployerNorthwestern University

Early life and education

Guillermo Oliver was born in 1955 in Montevideo, Uruguay.[1] He got his bachelor degree in Sciences from the University of Uruguay and his Master in Sciences degree from the National University of Mexico (UNAM).[2] He then completed his Ph.D work, focusing on the role of Hox genes in mouse development at UCLA.[3][4]

Career

Oliver has worked on cloning and characterizing the Six3 and Prox1 genes.[5] In 1996 he began working in the Department of Genetics at St. Jude Children's Research Hospital in Memphis, as a faculty member. [6][7] In 2015 he was named the Thomas D. Spies Professor of Lymphatic Metabolism at Northwestern University in the Department of Medicine in the Division of Nephrology and Hypertension, and he is also the director of the Center for Vascular and Developmental Biology at the Feinberg Cardiovascular Research Institute.[8]

Research

One of Oliver’s research focuses has been the lymphatic vasculature, and his laboratory demonstrated that Prox1 activity was required for the differentiation of lymphatic endothelial cells and the formation of the entire lymphatic vasculature.[9][10] They later showed the role of the lymphatic vasculature on obesity.[11][12] His laboratory also identified Six2 as a critical gene in the process of generation of nephron progenitors[13] and demonstrated that Six3 activity was required for the formation of the mammalian forebrain and neuroretina in mice.[14][15] He expanded those results using embryonic stem cells and induced pluripotent stem cells to generate eye organoids that mimic early eye development.[8]

Awards

In 2011 Oliver was elected to the American Association for the Advancement of Science in the Section on Biological Sciences.[6] Oliver was then elected a member of the Academia de Ciencias de América Latina in 2019.[1]

References
  1. "ACAL, Académicos 2019-2020 | ACAL". www.acal-scientia.org.
  2. Oliver, G., Gosset, G., Sanchez-Pescador, R., Lozoya, E., Ku Lailig, M.,Flores, N., Becerril, B., Valle, F., & Bolivar, F. (1987). Determination of the nucleotide sequence for the E. coli K12 Glutamate synthase structural genes. Gene 60, 1-11.
  3. De Robertis, E.M., Oliver, G., & Wright, C.V.E. (1990). Homeobox genes and the analysis of vertebrate development. Scientific American 263, 46-52.
  4. Oliver, G., Wright, C.V.E., Hardwicke, J., & De Robertis, E. (1988). A gradient of homeodomain protein in developing forelimbs of Xenopus and mouse embryos. Cell 55, 1017-1024
  5. Oliver, G., Sosa-Pineda, B., Geisendorf, S., Spana, E.P., Doe, C.Q., & Gruss, P. (1993). Prox1, a prospero-related homeobox gene expressed during mouse development. Mech Dev.44, 3-16.
  6. "AAAS Members Elected as Fellows | American Association for the Advancement of Science". www.aaas.org.
  7. "New insight offered in holoprosencephaly". UPI.
  8. Doss, Will. "Stem Cells Lead to Better Understanding of Retinal Development | Northwestern Medicine Magazine".
  9. Wigle, J.T. and Oliver, G. (1999). Prox1 function is required for the development of the murine lymphatic system. Cell 98, 769-778.
  10. Wigle, J.T., Harvey, N., Detmar, M., Lagutina, I., Grosveld, G., Gunn, M.D., Jackson, D.G., and Oliver, G. (2002). An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype. EMBO J 21, 1505-1513.
  11. "Leaky lymphatics lead to obesity in mice". ScienceDaily.
  12. Schneider, Martin; Conway, Edward M.; Carmeliet, Peter (October 15, 2005). "Lymph makes you fat". Nature Genetics. 37 (10): 1023–1024. doi:10.1038/ng1005-1023. PMID 16195715. S2CID 66017 – via www.nature.com.
  13. Self, M., Lagutin, O., Bowling, B., Hendrix, J., Cai, Y., Dressler, G. and Oliver, G. (2006). Six2 activity is required for suppression of inductive signals and progenitor cell renewal in the developing kidney. EMBO J, 25, 5214-28.
  14. Lagutin, O., Zhu, C., Kobayashi, D., Topczewski, J., Shimamura, K., Puelles, L., Russell, H.R., McKinnon, P., Solnica-Krezel, L. and Oliver, G. (2003). Six3 repression of Wnt signaling in the anterior neuroectoderm is essential for vertebrate forebrain development Genes & Dev 17, 368-379
  15. Liu, W., Lagutin, O., Swindell, E., Jamrich, M., and Oliver, G. (2010). Neuroretina specification in mammals requires Six3-mediated suppression of Wnt8b in the anterior neural plate. J Clin Invest, 120, 3568-3577.
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