THE AMOG BETA-2 SUBUNIT OF NA,K-ATPASE IS NOT NECESSARY FOR LONG-TERMSURVIVAL OF TELENCEPHALIC GRAFTS/

Adhesion molecule on glia (AMOG) represents the beta 2-subunit of muri ne Na,K-ATPase. Mice carrying a targeted deletion of the AMOG/beta 2 g ene exhibit tremor and limb paralysis at postnatal day (P) 15 and die 2 days after the onset of symptoms. The brains of these mice show edem a and swelling of astrocytic end feet. However, the cause of death has remained unclear. To identify long-term consequences of AMOG/beta 2 d eficiency, we have grafted parts of the embryonic telencephalic anlage of AMOG/beta 2-deficient mice into the caudoputamen of wild-type mice and analyzed the grafts up to 500 days after transplantation. Histolo gical, immunocytochemical, and in situ hybridization techniques were a pplied to examine histoarchitecture, proliferation, differentiation, a nd long-term survival of grafts. AMOG/beta 2-deficient telencephalic g rafts develop normally and form solid neural tissue that cannot be dis tinguished from control grafts by morphological features or with immun ocytochemical stains for neuronal and glial markers. No signs of degen eration can be found. Expression analysis, however, revealed that no A MOG/beta 2 protein of possible host origin can be detected in AMOG/bet a 2-deficient grafts. Graft-borne astrocytes express neither the AMOG/ beta 1 nor the AMOG/beta 2 subunit of Na,K-ATPase as examined with imm unocytochemistry and in situ hybridization. These findings indicate th at AMOG/beta 2 is not necessary for long-term survival of telencephali c graft tissue. (C) 1995 Wiley-Liss, Inc.