The years following the discovery of cyclin by Tim Hunt were filled with an abundance of discoveries relating to the cell cycle and its molecular processes.
Joan Ruderman, in collaboration with Katherine Swenson and Kevin Farrell, cloned the DNA coding for cyclin A from clam oocytes in 1986. They then created cyclin A mRNA in the lab and administered it to frog (Xenopus) oocytes which had been arrested at the border between gap 2 and meiosis I (Swenson, 1986: 861). The mRNA was translated by the frog oocytes and the resulting cyclin pushed the frog oocytes into meiosis. That indicated that cyclin A has some part in driving cells into meiosis.
Following his own work, Hunt began looking for ways to clone cyclin as well. With the ability to clone cyclin, and synthesize it in the lab, research with cyclin would expand dramatically. Hunt worked with molecular biologists Jeremy Minshull to clone cyclin B found in frog embryos (Jackson, 2008: 200). Once they had cloned cyclin B, they compared the DNA sequence of the cyclin A cloned by Ruderman and the cyclin B cloned by Hunt and Minshull and found that a particular part of the genetic code was conserved across both cyclins. That part was named the cyclin box (Jackson, 2008: 200).
At that point, in the late 1980s, it was yet unclear to researchers which was the major driver of mitosis - MPF or cyclin - though it was clear that both cyclin and MPF played a large role in the cell cycle. In particular, researchers did not know if it was the degradation of cyclin that caused a cell to exit mitosis or the degradation of MPF. In 1989, however, MBL researchers Marc Kirschner and Andrew Murray helped to answer that question. Using the cloned cyclin B from Hunt’s research, Murray and Kirschner showed that it was the degradation of cyclin that pushed the cell out of mitosis and that cyclin was the only required protein to cause a cell to enter into mitosis. That cemented cyclin’s role in the cell cycle, particularly as the main driver of mitosis (Pulverer, 2002).
Though cell cycle research had progressed significantly since Thomas Boveri’s work in 1902, many questions remained regarding the functioning of cyclin and its role in the cell cycle, such as the genetics behind cyclins and their functioning, and how cyclins are broken down in the cell in order to allow the cell to leave mitosis. Both of those questions were partially answered in the three years following Kirschner and Murray’s work.