Between February 1969 and August 1970 Edward Kollar and Grace Baird, from the University of Chicago in Chicago, Illinois, published three papers that established the role of the mesenchyme in tooth induction. Drawing upon a history of using tissue interactions to understand differentiation, Kollar and Baird designed their experiments to understand how differentiated structures become specified. Their work overturned a widely accepted model that epithelium controls the identity of the structure, a phenomenon called structural specificity. Interactions between epithelium and mesenchyme control the development and differentiation of many parts during embryonic development, including structures like the gastrointestinal tract and hair. Thus, the realization that mesenchyme drives induction and differentiation during epithelio-mesenchymal interactions had far-reaching effects.

In a series of experiments in the late 1970s, Alec J. Jeffreys in the UK and Richard A. Flavell in the Netherlands developed a technique to detect variations in the DNA of different individuals. They compared fragments of DNA from individuals’ beta-globin genes, which produce a protein in hemoglobin. Previously, to identify biological material, scientists focused on proteins rather than on genes. But evidence about proteins enabled scientists only to exclude, but not to identify, individuals as the sources of the biological samples. By 1979, Jeffrey’s experiments on beta-globin genes shifted the analytical approach of scientific identification from proteins to genes to identify an individual’s genetic identity. The ability to match a person to a biological sample developed in the 1980s and impacted many fields including paternity testing, forensics, immigration, and body identification.

In the US during the late 1960s, Stanley Alan Plotkin, John D. Farquhar, Michael Katz, and Fritz Buser isolated a strain of the infectious disease rubella and developed a rubella vaccine with a weakened, or attenuated, version of the virus strain. Rubella, also called German measles, is a highly contagious disease caused by the rubella virus that generally causes mild rashes and fever. However, in pregnant women, rubella infections can lead to developmental defects in their fetuses. Plotkin and his collaborators weakened a strain of rubella, called RA 27/3, by growing the virus in WI-38 cells, a strain of human embryonic cells developed at the Wistar Institute by Leonard Hayflick in the early 1960s. Their research led to the development of a rubella vaccine, which prevented rubella in children and congenital rubella syndrome in the fetuses of pregnant women who had contracted rubella.

In 1995, researchers Ann Burke, Craig Nelson, Bruce Morgan, and Cliff Tabin in the US studied the genes that regulate the construction of vertebra in developing chick and mouse embryos, they showed similar patterns of gene regulation across both species, and they concluded that those patterns were inherited from an ancestor common to all vertebrate animals. The group analyzed the head-to-tail (anterior-posterior) axial development of vertebrates, as the anterior-posterior axis showed variation between species over the course of evolutionary time. Along those axes, they showed where Hox genes produced RNAs. Hox genes have the homeobox, a portion of DNA contributes to the generation of the body plans of animals, plants, and fungi. In the 1995 study, the researchers compared the expression patterns of Hox genes across the chick and mouse embryos, showing where the patterns were similar and where they differed. Based on those comparisons, they argued that Hox genes were present in the ancestors of tetrapods and fishes, and that Hox genes function in the segmentation of the anterior-posterior vertebrate axis in both chick and mouse embryos.

Barbara McClintock conducted experiments on corn (Zea mays) in the United States in the mid-twentieth century to study the structure and function of the chromosomes in the cells. McClintock researched how genes combined in corn and proposed mechanisms for how those interactions are regulated. McClintock received the Nobel Prize in Physiology or Medicine in 1983, the first woman to win the prize without sharing it. McClintock won the award for her introduction of the concept of transposons, also called jumping genes. McClintock conceptualized some genetic material as not static in structure and order, but as subject to re-arrangement and may be altered during development.

Leonard Hayflick in the US during the early 1960s showed that normal populations of embryonic cells divide a finite number of times. He published his results as 'The Limited In Vitro Lifetime of Human Diploid Cell Strains' in 1964. Hayflick performed the experiment with WI-38 fetal lung cells, named after the Wistar Institute, in Philadelphia, Pennsylvania, where Hayflick worked. Frank MacFarlane Burnet, later called the limit in capacity for cellular division the Hayflick Limit in 1974. In the experiment, Hayflick refuted Alexis Carrel's hypothesis that cells could be transplanted and multiplied indefinitely from a single parent cell line.

In 1893, Julia Barlow Platt published her research on the origins of cartilage in the developing head of the common mudpuppy (Necturus maculosus) embryo. The mudpuppy is an aquatic salamander commonly used by embryologists because its large embryonic cells and nuclei are easy to see. Platt followed the paths of cells in developing mudpuppy embryos to see how embryonic cells migrated during the formation of the head. With her research, Platt challenged then current theories about germ layers, the types of cells in an early embryo that develop into adult cells. In most organisms' development, three types of germ layers are responsible for the formation of tissues and organs. The outermost layer is called ectoderm, the middle layer mesoderm, and the innermost layer endoderm, although Platt called it entoderm. Platt's research provided a basis for scientists to clarify the destination or function of the germ layers in vertebrates' development.

In the late 1990s researchers Yuk Ming Dennis Lo and his colleagues isolated fetal DNA extracted from pregnant woman’s blood. The technique enabled for more efficient and less invasive diagnoses of genetic abnormalities in fetuses, such as having too many copies of chromosomes. Lo’s team published their results in 1997’s “Presence of Fetal DNA in Maternal Plasma and Serum.” The results led to developments of clinical tests that can access fetal genetic information and detect genetic abnormalities before birth without the significant risks that can potentially harm the fetus associated with invasive genetic testing techniques.

In 1962 researcher John Bertrand Gurdon at the University of Oxford in Oxford, England, conducted a series of experiments on the developmental capacity of nuclei taken from intestinal epithelium cells of feeding tadpoles. In the experiments, Gurdon conducted nuclear transplantation, or cloning, of differentiated cells, or cells that have already specialized to become one cell type or another, in tadpoles. Gurdon's experiment showed that differentiated adult cells could be induced to an undifferentiated state, where they could once again become multiple cell types. Gurdon's experiment disproved the theory that differentiated cells could not be undifferentiated or dedifferentiated into a new type of differentiated cell. Gurdon's experiment demonstrated nuclear transplantation, also called cloning, using differentiated cells.

From 1977 to 1987, Harald zur Hausen led a team of researchers across several institutions in Germany to investigate whether the human papillomavirus (HPV) caused cervical cancer. Zur Hausen's first experiment tested the hypothesis that HPV caused cervical cancer rather than herpes simplex virus type 2 (HSV-2), the then accepted cause. His second and third experiments detailed methods to identify two previously unidentified HPV strains, HPV 16 and HPV 18, in cervical cancer tumor samples. The experiments showed that HPV 16 and 18 DNA were present in cervical tumor samples. Zur Hausen concluded that HPV, not HSV-2, caused cervical cancer, which enabled researchers to develop preventions, such as the HPV vaccine.