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

• Published in: Development (Cambridge) Vol. 126; no. 7; pp. 1365 - 1374
• Main Authors: Roth, L W, Bormann, P, Bonnet, A, Reinhard, E
• Format: Journal Article
• Language: English
• Published: England The Company of Biologists Limited 01.04.1999
• Subjects: Amino Acid Sequence; Animals; Axons - metabolism; Base Sequence; Brain - embryology; Cloning, Molecular; Danio rerio; Freshwater; Gene Expression Regulation, Developmental - genetics; Homeodomain Proteins - genetics; Immunohistochemistry; In Situ Hybridization; LIM-Homeodomain Proteins; Molecular Sequence Data; Muscles - embryology; Nerve Tissue Proteins; Nervous System - embryology; RNA - genetics; RNA, Antisense - pharmacology; Sequence Alignment; Thymosin - chemistry; Thymosin - genetics; Transcription Factors; Zebrafish - embryology; Zebrafish - genetics
• ISSN: 0950-1991; 1477-9129
• DOI: 10.1242/dev.126.7.1365

beta-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 beta-thymosin during differentiation, coinciding with the time of innervation. Injection of beta-thymosin antisense RNA into zebrafish 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, antisense-injected 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 beta-thymosin may be involved in the maintenance of the expression of molecules necessary for neuronal differentiation. Taken together, our results strongly indicate that beta-thymosin is an important regulator of development.