The Edinburgh Mouse Atlas, also called the e-Mouse Atlas Project (EMAP), is an online resource comprised of the e-Mouse Atlas (EMA), a detailed digital model of mouse development, and the e-Mouse Atlas of Gene Expression (EMAGE), a database that identifies sites of gene expression in mouse embryos. Duncan Davidson and Richard Baldock founded the project in 1992, and the Medical Research Council (MRC) in Edinburgh, United Kingdom, funds the project. Davidson and Baldock announced the project in an article titled A Real Mouse for Your Computer, citing the need to manage and analyze the volume of data that overwhelmed developmental biologists. Though EMAP resources were distributed via CD-ROM in the early years, the project moved increasingly online by the early 2000s, and into the early decades of the twenty-first century, was in active development. EMAP can be utilized as a developmental biology teaching resource and as a research tool that enables scientists to explore annotated 3D virtual mouse embryos. EMAP's goal is to illuminate the molecular basis of tissue differentiation.

In 2003, molecular biology and genetics researchers Coleen T. Murphy, Steven A. McCarroll, Cornelia I. Bargmann, Andrew Fraser, Ravi S. Kamath, Julie Ahringer, Hao Li, and Cynthia Kenyon conducted an experiment that investigated the cellular aging in, Caenorhabditis elegans (C. elegans) nematodes. The researchers investigated the interactions between the transcription factor DAF-16 and the genes that regulate the production of an insulin-like growth factor 1 (IGF-1-like) protein related to the development, reproduction, and aging in C. elegans. Transcription factors, like DAF-16, are proteins that regulate the transcription of deoxyribonucleic acid (DNA) into messenger ribonucleic acid (mRNA), which later determines which proteins the cell produces. The research team's experiment suggested that an increase in the activity of the DAF-16 protein decreases the transcription of the genes that regulate the production of IGF-1-like proteins, increasing lifespan in nematodes. The team published their results in the article 'Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans' in Nature in June 2003. By comparing the regulation of gene expression in C. elegans with similar genes and pathways in humans, Murphy's research team sought to better understand cellular function and aging in humans.

In 1961, Mary Lyon, a researcher who studied genetics, published “Gene Action in the X-chromosome of the Mouse (Mus Musculus L.),” hereafter “Gene Action in the X-chromosome,” in the journal Nature. Lyon’s paper focuses on the workings of female sex chromosomes, or X-chromosomes, and their implications for gene expression. A chromosome is a structure in a cell’s nucleus that contains the DNA, or genetic information, for each individual. In her paper, Lyon proposes her X-inactivation hypothesis, which states that one of the two X-chromosomes in mammalian female cells becomes inactive during early development, silencing its genetic activity. By describing X-chromosome inactivation, Lyon provided an explanation for the mosaic patterns observed in some female mammals, where different regions of their bodies exhibit distinct traits based on the genes carried by the particular X-chromosome that is active in that region. “Gene Action in the X-chromosome” provided evidence that X-chromosome inactivation occurs, laying the basis for understanding sex-linked traits, gene expression, and X-linked genetic diseases that impact thousands of people.

Mary Frances Lyon studied gene expression and developed the theory of X-chromosome inactivation, also called Lyonization, during the twentieth century in the United Kingdom. The Lyonization hypothesis proposes that, even though females have two X-chromosomes and males have only one, one X-chromosome in females is always randomly inactivated, which causes males and females to have the same level of X-chromosome gene expression. Prior to Lyon’s hypothesis, scientists understood that there must be a biological way to compensate for the difference in X-chromosomes in males and females, but they did not know the exact mechanism. To investigate the topic, Lyon studied coat color in mice, a trait influenced by genes on the X-chromosome. Her resulting hypothesis highlighted X-chromosome inactivation as a mechanism for controlling gene expression in females without altering their DNA sequence. Through her research, Lyon aided scientists in understanding X-linked disorders, which laid the foundation for the development of gene therapies designed to treat X-linked disorders that affect hundreds of thousands of people globally.