In 2002 Eric Davidson and his research team published 'A Genomic Regulatory Network for Development' in Science. The authors present the first experimental verification and systemic description of a gene regulatory network. This publication represents the culmination of greater than thirty years of work on gene regulation that began in 1969 with 'A Gene Regulatory Network for Development: A Theory' by Roy Britten and Davidson. The modeling of a large number of interactions in a gene network had not been achieved before. Furthermore, this model revealed behaviors of the gene networks that could only be observed at the levels of biological organization above that of the gene.

Victor Ambros is a professor of molecular medicine at the University of Massachusetts Medical School, and he discovered the first microRNA (miRNA) in 1993. Ambros researched the genetic control of developmental timing in the nematode worm Caenorhabditis elegans and he helped describe gene function and regulation during the worm’s development and embryogenesis. His discovery of miRNA marked the beginning of research into a form of genetic regulation found throughout diverse life forms from plants to humans. Ambros is a central figure in the miRNA and C. elegans research communities, and co-directs the RNA Therapeutics Institute.

As mice embryos develop, they undergo a stage of development called gastrulation. The hallmark of vertebrate gastrulation is the reorganization of the inner cell mass (ICM) into the three germ layers: ectoderm, mesoderm, and endoderm. Mammalian embryogenesis occurs within organisms; therefore, gastrulation was originally described in species with easily observable embryos. For example, the African clawed frog (Xenopus laevis) is the most widely used organism to study gastrulation because the large embryos develop inside a translucent membrane. Domestic chicken (Gallus gallus) gastrulation was also an early model organism because researchers could open the egg during development to look inside. Despite the challenges associated with studying mammalian gastrulation, the common house mouse (Mus musculus) has helped to shed light on the unique adaptations associated with mammalian development, and on the subtle differences in structure that give rise to significant divergence in late embryogenesis.

Implantation is a process in which a developing embryo, moving as a blastocyst through a uterus, makes contact with the uterine wall and remains attached to it until birth. The lining of the uterus (endometrium) prepares for the developing blastocyst to attach to it via many internal changes. Without these changes implantation will not occur, and the embryo sloughs off during menstruation. Such implantation is unique to mammals, but not all mammals exhibit it. Furthermore, of those mammals that exhibit implantation, the process differs in many respects between those mammals in which the females have estrous cycles, and those mammals in which the femals have menstrual cycles. Females in the different species of primates, including humans, have menstrual cycles, and thus similar processes of implantation.

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.