Abstract
β-Thymosins are polypeptides that bind monomeric actin and thereby function as actin buffers in many cells. We show that during zebrafish development, β-thymosin expression is tightly correlated with neuronal growth and differentiation. It is transiently expressed in a subset of axon-extending neurons, essentially primary neurons that extend long axons, glia and muscle. Non-neuronal expression in the brain is restricted to a subset of glia surrounding newly forming axonal tracts. Skeletal muscle cells in somites, jaw and fin express β-thymosin during differentiation, coinciding with the time of innervation. Injection of β-thymosin antisense RNA into zebrafish embryos results in brain defects and impairment of the development of β-thymosin-associated axon tracts.
Furthermore, irregularities in somite formation can be seen in a subset of embryos. Compared to wild-type, antisenseinjected embryos show slightly weaker and more diffuse engrailed staining at the midbrain-hindbrain boundary and a strong reduction of Isl-1 labeling in Rohon Beard and trigeminal neurons. The decreased expression is not based on a loss of neurons indicating that β-thymosin may be involved in the maintenance of the expression of molecules necessary for neuronal differentiation. Taken together, our results strongly indicate that β-thymosin is an important regulator of development.
