Abstract

Fibroblast growth factor-16 (FGF-16) is important for the growth and development of the embryonic myocardium in mice. Disruption of Fgf-16 effects cardiac development; however, the severity of the defects varies in different strains of mice. Lu et al. investigate the role of host genetics in the phenotypes of Fgf-16 knockout mice in their article, “Embryonic Survival and Severity of Cardiac and Craniofacial Defects Are Affected by Genetic Background in Fibroblast Growth Factor-16 Null Mice.” They found that after three generations, back-crossing a Fgf-16 mutation into C57BL/6 mice led to survival of about 25% of potential Fgf-16 null mice while no Fgf-16 Black Swiss null mice survived. Lu and colleagues also found that FGF-8 RNA levels were reduced in Black Swiss, but not C57BL/6 mice. Basal expression levels of related genes also varied between mouse strains. Host modulation of gene expression may partially explain the differences in phenotypes seen in various lines of Fgf-16 knockout mice.
