TGFβ1a regulates zebrafish posterior lateral line formation via Smad5 mediated pathway.

Overview

The zebrafish sensory posterior lateral line (pLL) has become an attractive model for studying collective cell migration and cell morphogenesis. Recent studies have indicated that chemokine, Wnt/β-catenin, Fgf, and Delta-Notch signaling pathways participate in regulating pLL development. However, it remains unclear whether TGFβ signaling pathway is involved in pLL development. Here we report a critical role of TGFβ1 in regulating morphogenesis of the pLL primordium (pLLP). The tgfβ1a gene is abundantly expressed in the lateral line primordium. Knockdown or knockout of tgfβ1a leads to a reduction of neuromast number, an increase of inter-neuromast distance, and a reduced number of hair cells. The aberrant morphogenesis in embryos depleted of tgfβ1a correlates with the reduced expression of atoh1a, deltaA, and n-cadherin/cdh2, which are known important regulators of the pLLP morphogenesis. Like tgfβ1a depletion, knockdown of smad5 that expresses in the pLLP, affects pLLP development whereas overexpression of a constitutive active Smad5 isoform rescues the defects in embryos depleted of tgfβ1a, indicating that Smad5 mediates tgfβ1a function in pLLP development. Therefore, TGFβ/Smad5 signaling plays an important role in the zebrafish lateral line formation.