Mice develop normally without tenascin.

TLDR

Tenascin is an extracellular matrix protein expressed in a restricted pattern during embryogenesis and has been implicated in various morphogenetic processes. The study aimed to directly test tenascin’s role in vivo by creating mice in which the tenascin gene was replaced with lacZ. In the mutant mice, lacZ expression replaced tenascin and no tenascin protein was detected. Homozygous mutants were viable, fertile, showed no anatomical or histological defects, and displayed normal distribution of other extracellular matrix components, calling into question tenascin’s essential role in development.

Abstract

Tenascin, an extracellular matrix protein, is expressed in an unusually restricted pattern during embryogenesis and has been implicated in a variety of morphogenetic phenomena. To directly assess the function of tenascin in vivo, we generated mutant mice in which the tenascin gene was nully disrupted by replacing it with the lacZ gene. In mutant mice, lacZ was expressed in place of tenascin, and no tenascin product was detected. Homozygous mutant mice were, however, obtained in accordance with Mendelian laws, and both females and males produced offspring normally. No anatomical or histological abnormalities were detected in any tissues, and no major changes were observed in distribution of fibronectin, laminin, collagen, and proteoglycan. The existence of these mutant mice, lacking tenascin yet phenotypically normal, casts doubt on the theory that tenascin plays and essential role in normal development.