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Tardigrades are microscopic animals that can survive exceptional levels of ionizing radiation or desiccation—DNA-damaging conditions that would kill most animals. Irradiation or radiomimetic drug treatment of the tardigrade Hypsibius exemplaris can induce remarkably high expression levels of DNA repair genes, primarily those in the base excision repair and nonhomologous end joining pathways. How tardigrades can repair widespread DNA damage without producing frequent, large-scale chromosome structural abnormalities, like chromosome translocations and fusions, is unknown. Here, we report the results of examining chromosome and nuclear architecture throughout the cell cycle in early embryos of H. exemplaris. We found that H. exemplaris chromosomes are maintained in an individualized form throughout the cell cycle. We were surprised to also find that each chromosome is housed in a fully or partially separate lamin-lined compartment, instead of all chromosomes being housed in a single, nearly spherical nuclear lamina and envelope. Our results reveal unusual chromosomal and nuclear organization in a tardigrade. We speculate that these unexpected features might limit chromosomal rearrangements during DNA damage repair in extreme conditions. 

Although synaptic evolution has been extensively studied, how axons first arose remains unexplored. Because evolution often occurs by coopting existing features, we review the evolutionary histories, biophysics, and cell biology of cytokinesis, cell crawling, and ciliogenesis to explore the origin of axons. Although we found that cilia and axons are outwardly similar, and growth cones strongly resemble the leading edge of crawling cells, the biophysical processes and the critical proteins that drive each seem weakly linked to axons as a structure. In contrast, the traction force machinery that pulls daughter cells apart during cytokinesis and the cytoskeletal organization of cytokinetic bridges appear to have a one-to-one correspondence to neuronal growth cones and axons. Based on these observations, we propose the hypothesis that axons evolved due to mutations that partially activated cytokinesis in an interphase cell. To rigorously test this hypothesis, we suggest conducting systematic phylogenetic analysis of the genes essential for each process, paired with molecular genetic studies in which critical genes are systematically disrupted. Doing so will provide a framework for understanding the relationship between diverse cellular processes, the early evolution of neurons, and insights that could potentially assist in treating cancer and promoting neuronal regeneration.