Two molecular models of initial left-right asymmetry generation

Med Hypotheses. 1997 Nov;49(5):429-35. doi: 10.1016/s0306-9877(97)90092-x.

Abstract

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.

MeSH terms

  • Animals
  • Body Patterning* / genetics
  • Connexin 43 / physiology
  • Dyneins / physiology
  • Humans
  • Models, Molecular*

Substances

  • Connexin 43
  • Dyneins