Regulation of acetylcholine receptor gene expression in rats treated with alpha-bungarotoxin.
Regulation of acetylcholine receptor (AChR) gene expression was analyzed in alpha-bungarotoxin (alpha-BTX) treated rats. A reduction in available 125I-alpha-BTX binding sites was accompanied by an increase in the various AChR transcripts. The increase in the AChR alpha-, beta- epsilon- and delta-subunit mRNAs was similar to that observed in rats with experimental autoimmune myasthenia gravis (EAMG). Unlike in EAMG, the gamma-subunit transcripts reappeared following alpha-BTX treatment. The quantitative differences in the levels of AChR transcripts between alpha-BTX treatment and EAMG on one hand and denervation on the other hand, support the notion that the regulation of AChR gene expression is controlled by muscle activity and by neuronal factors as well. We also demonstrate in this report that myogenin transcripts increase following alpha-BTX treatment as well as following denervation, whereas MyoD1 transcripts remain stable.
Asher
O
O
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
Provenzano
C
C
Fuchs
S
S
D000199:Actins / Q000235:genetics; D000818:Animals; D015152:Blotting, Northern; D002038:Bungarotoxins / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects*; D009121:Muscle Denervation; D009124:Muscle Proteins / Q000235:genetics; D017570:MyoD Protein; D018008:Myogenin; D009687:Nuclear Proteins / Q000235:genetics; D010750:Phosphoproteins / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011917:Rats, Inbred Lew; D011978:Receptors, Nicotinic / Q000235:genetics*; D013997:Time Factors
D000199:Actins; D002038:Bungarotoxins; D009124:Muscle Proteins; D017570:MyoD Protein; C057363:MyoD1 myogenic differentiation protein; C503803:Myog protein, rat; D018008:Myogenin; D009687:Nuclear Proteins; D010750:Phosphoproteins; D012333:RNA, Messenger; D011978:Receptors, Nicotinic