Embryo Project Encyclopedia Articles

Sir John Bertrand Gurdon further developed nuclear transplantation, the technique used to clone organisms and to create stem cells, while working in Britain in the second half of the twentieth century. Gurdon's research built on the work of Thomas King and Robert Briggs in the United States, who in 1952 published findings that indicated that scientists could take a nucleus from an early embryonic cell and successfully transfer it into an unfertilized and enucleated egg cell. Briggs and King also concluded that a nucleus taken from an adult cell and similarly inserted into an unfertilized enucleated egg cell could not produce normal development. In 1962, however, Gurdon published results that indicated otherwise. While Briggs and King worked with Rana pipiens frogs, Gurdon used the faster-growing species Xenopus laevis to show that nuclei from specialized cells still held the potential to be any cell despite its specialization. In 2012, the Nobel Prize Committee awarded Gurdon and Shinya Yamanaka its prize in physiology and medicine for for their work on cloning and pluripotent stem cells.

Among other functions, the Notch signaling pathway forestalls the process of myogenesis in animals. The Notch signaling pathway is a pathway in animals by which two adjacent cells within an organism use a protein named Notch to mechanically interact with each other. Myogenesis is the formation of muscle that occurs throughout an animal's development, from embryo to the end of life. The cellular precursors of skeletal muscle originate in somites that form along the dorsal side of the organism. The Notch signaling pathway is active in multiple aspects of somitogenesis, and it continues to be a critical regulator during myogenesis. Throughout the life of an organism, Notch signaling prevents the differentiation of muscle progenitor cells into muscle cells. Such preventions help maintain populations of progenitor cells that can remain dormant until the growth or repair of muscle is necessary, at which point the Notch signal to the muscle progenitor cells is disrupted, and the muscle progenitor cells differentiate into muscle fibers and cells. Without Notch signaling, myogenesis proceeds prematurely and dissipates before mature muscle can form.