I read Biochemistry as an undergraduate at University College London, and have been studying long-bone growth since 2012 when I began my PhD at the University of Manchester and Roslin Institute (Edinburgh, UK). I then moved to Karolinska Institute and conducted postdoctoral research with Asst. Professor Andrei Chagin (Department of Physiology and Pharmacology), during which time I was also associated with Prof. Lars Sävendahl's lab (Department of Women's and Children's Health). Since January 2020, I moved to the Department of Women's and Children's Health where I have started working as a principle investigator in the group of Prof. Klas Blomgren.
Until we reach our adult height, our long-bones are being continuously lengthened because of the activity of narrow discs of cartilage in our long-bones, called growth plates. Growth plates are very interesting tissues. Each growth plate is made up of highly organised columns of cells (chondrocytes), in which the last cell in the column is continually removed and replaced by bone tissue. This process must be very tightly controlled so that our bones continue to grow in proportion to each other and so that we grow similarly to our peers. Long-bone growth is important as it ultimately determines how tall we become.
My research aims to understand the fundamental aspects of long-bone growth at the cellular level and to unravel the signaling pathways controlling this process. By coupling clinical samples with basic research at the lab bench we endeavour to have a patient-oriented approach.
(1) A radical switch in clonality reveals a stem cell niche in the epiphyseal growth plate. Newton PT, Li L, Zhou B, Schweingruber C, Hovorakova M, Xie M, Sun X, Sandhow L, Artemov AV, Ivashkin E, Suter S, Dyachuk V, El Shahawy M, Gritli-Linde A, Bouderlique T, Petersen J, Mollbrink A, Lundeberg J, Enikolopov G, Qian H, Fried K, Kasper M, Hedlund E, Adameyko I, Sävendahl L, Chagin AS; Nature 567(7747):234-238 (2019)
(2) Superficial cells are self-renewing chondrocyte progenitors, which form the articular cartilage in juvenile mice. Li L*, Newton PT*, Bouderlique T, Sejnohova M, Zikmund T, Kozhemyakina E, Xie M, Krivanek J, Kaiser J, Qian H, Dyachuk V, Lassar AB, Warman ML, Barenius B, Adameyko I, Chagin AS; FASEB 31(3):1067-1084 (2016)
(3) Pharmacological inhibition of lysosomes activates the mTORC1 signaling pathway in chondrocytes in an autophagy-independent manner. Newton PT*, Vuppalapati KK*, Bouderlique T, Chagin AS; Autophagy 11(9):1594-607 (2015)
(4) Clonal Genetic Tracing using the Confetti Mouse to Study Mineralized Tissues. Zhou B, Kaucka M, Chagin AS, Newton PT; J. Vis. Exp. (152), e60424, doi:10.3791/60424 (2019)
(5) New insights into niclosamide action: autophagy activation in colorectal cancer (Commentary). Newton PT; Biochem J. 476(5):779-781 (2019)
(6) Chondrogenic ATDC5 cells: an optimised model for rapid and physiological matrix mineralization. Newton PT*, Staines KA*, Spevak L, Boskey AL, Teixeira CC, Macrae VE, Canfield AE, Farquharson C; Int J Mol Med 30(5):1187-93 (2012)
(7) Novel KIAA0753 mutations extend the phenotype of skeletal ciliopathies. Hammarsjö A, Wang Z, Vaz R, Taylan F, Sedghi M, Girisha KM, Chitayat D, Neethukrishna K, Godoy R, Gowrishankar K, Lindstrand A, Nasiri J, Baktashian M, Newton PT, Guo L, Hofmeister W, Petterson M, Chagin AS, Nishimura G, Yan L, Matsumoto N, Shannon P, Nordgren A, Miyake N, Grigelioniene G, Ikegawa S; Scientific Reports 7(1):15585 (2017)
* denotes shared first authorship.
Academic honours, awards and prizes
Harold M. Frost Young Investigator Award (2019)
American Society for Bone and Mineral Research Young Investigator Award (2016)