Left-right (LR) asymmetry is a fascinating problem in embryonic morpho
genesis. Recently, a pathway of genes has been identified which is inv
olved in LR patterning in vertebrates. Although this work characterize
s the interactions of several asymmetrically-expressed genes, it is st
ill entirely unclear how such asymmetric expression is set up in the f
irst place. There are two promising molecular candidates which may pla
y a role is such a process: the motor protein dynein, and the gap junc
tion protein connexin-43 (Cx43). We present two models, significantly
supported by previous findings, which hypothesize that (a) dynein asym
metrically localizes LR determinants in individual cells to establish
cell-autonomous LR biasing, and (b) asymmetric activity of Cx43 gap ju
nctions within key cells sets up electric potentials in multicellular
fields, thus establishing large-scale LR asymmetry.