beta-thymosin is required for axonal tract formation in developing zebrafish brain

Citation
Lwa. Roth et al., beta-thymosin is required for axonal tract formation in developing zebrafish brain, DEVELOPMENT, 126(7), 1999, pp. 1365-1374
Citations number
57
Categorie Soggetti
Cell & Developmental Biology
Journal title
DEVELOPMENT
ISSN journal
09501991 → ACNP
Volume
126
Issue
7
Year of publication
1999
Pages
1365 - 1374
Database
ISI
SICI code
0950-1991(199904)126:7<1365:BIRFAT>2.0.ZU;2-D
Abstract
beta-Thymosins are polypeptides that bind monomeric actin and thereby funct ion as actin buffers in many cells. We show that during zebrafish developme nt, beta-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 musc le. 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 beta-thymosin during differentiation, coinciding with t he time of innervation. Injection of beta-thymosin antisense RNA into zebra fish embryos results in brain defects and impairment of the development of beta-thymosin-associated axon tracts. Furthermore, irregularities in somite formation can be seen in a subset of embryos. Compared to wild-type, antis ense-injected embryos show slightly weaker and more diffuse engrailed stain ing at the midbrain-hindbrain boundary and a strong reduction of Isl-1 labe ling in Rohon Beard and trigeminal neurons. The decreased expression is not based on a loss of neurons indicating that beta-thymosin may be involved i n the maintenance of the expression of molecules necessary for neuronal dif ferentiation. Taken together, our results strongly indicate that beta-thymo sin is an important regulator of development.