Here, I characterize a symbiotic mutant of Lotus japonicus, called sunergos1 (suner1), which originated from a har1-1 suppressor screen. I have shown that suner1 supports epidermal infection by rhizobia and initiates nodule primordia organogenesis as in wild-type. However, the infection process is temporarily stalled, such that infection threads fail to ramify within the root cortex and timely release of bacteria inside the nodule primordia cells does not occur. This symbiotic defect is ephemeral and with additional time, functional nodules are formed. Using a combined approach involving map-based cloning and next-generation sequencing, I have shown that the suner1 phenotype is determined by a recessive mutant allele, with the corresponding wild-type SUNER1 locus encoding a predicted subunit A of a DNA topoisomerase VI. The data obtained suggest that the SUNER1 topoisomerase VI mediates endoreduplication of nodule primordia cells and that this is essential for normal differentiation of functional, nitrogen-fixing nodules