While components of the pathway that establishes left-right asymmetry have been 
identified in diverse animals, from vertebrates to flies, it is striking that 
the genes involved in the first symmetry-breaking step remain wholly unknown in 
the most obviously chiral animals, the gastropod snails. Previously, research on 
snails was used to show that left-right signaling of Nodal, downstream of 
symmetry breaking, may be an ancestral feature of the Bilateria [1 and 2]. Here, 
we report that a disabling mutation in one copy of a tandemly duplicated, 
diaphanous-related formin is perfectly associated with symmetry breaking in the 
pond snail. This is supported by the observation that an anti-formin drug 
treatment converts dextral snail embryos to a sinistral phenocopy, and in frogs, 
drug inhibition or overexpression by microinjection of formin has a 
chirality-randomizing effect in early (pre-cilia) embryos. Contrary to 
expectations based on existing models [3, 4 and 5], we discovered asymmetric 
gene expression in 2- and 4-cell snail embryos, preceding morphological 
asymmetry. As the formin-actin filament has been shown to be part of an 
asymmetry-breaking switch in vitro [6 and 7], together these results are 
consistent with the view that animals with diverse body plans may derive their 
asymmetries from the same intracellular chiral elements [8].