Neurons polarize by forming a single axon and multiple dendrites. Neuronal functions depend on their robust polarity. However, the mechanisms that ensure generation and maintenance of only a single axon remain poorly understood. We have reported a RUN domain-containing protein, named singar1 (single axon-related 1), whose expression became up-regulated during polarization of cultured hippocampal neurons. Reduction of the expression of singar1 by RNAi led to an increase in the population of neurons bearing surplus axons. Conversely, overexpression of singar1 did not affect normal neuronal polarization but suppressed the formation of surplus axons induced by excess levels of shootin1, a recently identified protein involved in neuronal polarization. We proposed that singar1 ensures the robustness of neuronal polarity by suppressing formation of surplus axons. However the in vivo function of singar1 is unknown.
Here, we show the in vivo function of singar1 using singar knockout mice. Mouse singar1 were only detected in the brain and not in the other organs. Singar knockout mice showed no suckling response and died shortly after birth. However, we did not observe any signs of the digestive organs.