In vivo live image of Musashi2-reporter KPf/fC pancreas tumor. Blood vessels are marked with anti-VE-cadherin antibody (magenta), nuclei are marked by Hoechst (blue), and endogenous Musashi2-reporter is shown in green.
Miyamoto Musashi was one of Japan’s greatest samurais (Yoshikawa 1981). Known for his exceptional talent as a warrior, Musashi developed a unique way of fighting with two swords: a long sword, or katana, and a short sword, or wakizashi. The two-sword technique used by Musashi was termed Niten Ichi Ryu (two heavens as one) or Nito Ryu (the school of the two swords). Musashi combined his keen interest in combat with an interest in philosophy and Zen Buddhism, going on to write several books on strategy that have had an enduring appeal for both the Eastern and Western worlds.
Although iconic in Japanese history and culture, Musashi’s name and unique story became part of the scientific lexicon serendipitously. In the early 1990s, a group of scientists led by noted neurobiologist Craig Montell discovered a new gene, which, when mutated, led to a cell fate determination defect in sensory organ precursor cells. In Drosophila, the sensory organ precursor cells give rise to the ectodermal system and can generate both neural and non-neural cell lineages. Normally these cells give rise to a IIa non-neuronal precursor cell, which goes on to make the socket and shaft of a bristle, and a IIb neuronal precursor cell, which goes on to make a neuron and glia. However, in this mutant, two identical non-neural precursor cells were generated, which frequently differentiated into two shaft-forming cells resulting in a double-bristle phenotype. Because the two-bristle phenotype was reminiscent of the great samurai’s two swords, the gene was named Musashi (Nakamura et al. 1994). Musashi, the family of RNA-binding proteins encoded by the Musashi gene, has emerged as a key signal that confers and protects the stem cell state across organisms, and its reactivation can be a critical element in oncogenesis.