Lessons from genetic knockout mice deficient in neural recognition molecules

The chapter describes the experience with genetic knockout mutants of the mouse deficient in three neural recognition molecules: (1) the major peripheral myelin glycoprotein of mammals, the immunoglobulin superfamily-derived recognition molecule PO, (2) the adhesion molecule on glia (AMOG), a recognition molecule and the integral component of the Na,K-ATPase, and (3) the minor glycoprotein of central and peripheral nervous system myelin-forming cells, the myelin-associated glycoprotein (MAG). All three molecules are mostly expressed in the nervous system and therein predominantly produced by glial cells at later stages of their development. The spatial and temporal restriction in expression is beneficial for the production of a viable mutant animal. Analysis of the three mutants shows the range of phenotypes that can be expected from general considerations on knockout strategies. The findings carry implications for future strategies intended to elucidate the functional role of a neural recognition molecule by genetic ablation.