Two molecular models of initial left-right asymmetry generation.
Left-right (LR) asymmetry is a fascinating problem in embryonic morphogenesis. Recently, a pathway of genes has been identified which is involved in LR patterning in vertebrates. Although this work characterizes the interactions of several asymmetrically-expressed genes, it is still entirely unclear how such asymmetric expression is set up in the first place. There are two promising molecular candidates which may play a role is such a process: the motor protein dynein, and the gap junction protein connexin-43 (Cx43). We present two models, significantly supported by previous findings, which hypothesize that (a) dynein asymmetrically localizes LR determinants in individual cells to establish cell-autonomous LR biasing, and (b) asymmetric activity of Cx43 gap junctions within key cells sets up electric potentials in multicellular fields, thus establishing large-scale LR asymmetry.
Levin
M
M
Cell Biology Department, Harvard Medical School, Boston, MA 02115, USA. mlevin@husc.harvard.edu
Nascone
N
N
D000818:Animals; D019521:Body Patterning / Q000235:genetics; D018031:Connexin 43 / Q000502:physiology; D004398:Dyneins / Q000502:physiology; D006801:Humans; D008958:Models, Molecular
D018031:Connexin 43; D004398:Dyneins