Tubulin is a major cytoskeletal component and, at first glance, might seem unconnected to mRNA decay. Yet, a 1987 paper from Don Cleveland and colleagues established the central role of mRNA decay in controlling the abundance of free tubulin, though it would take nearly four decades before the underlying mechanisms were fully elucidated.

α- and β-tubulin subunits form heterodimers, which are the building blocks of microtubules. Proper expression of these subunits is needed for a variety of fundamental cellular processes, such as chromosome segregation during mitosis, and is highly regulated between different cell types. Adding to the biological complexity is the dynamic nature of microtubules, which can rapidly (de)polymerize in response to different stresses and signals. Moreover, many genomes encode paralogous genes, which must be co-ordinated as a group to ensure correct tubulin levels. On the basis of work in the 1970s and early 1980s, it became clear that one important aspect of tubulin regulation is a negative feedback loop whereby excess subunits lead to degradation of tubulin-encoding mRNAs, but the molecular mechanism was unknown.