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ISSN 0582-9879 Acta Biochim et Biophysica Sinica 2004, 36(6):412-418 CN 31-1300/Q


Characterization of MR-1, a Novel Myofibrillogenesis Regulator in Human Muscle

Tian-Bo LI, Xiu-Hua LIU1, Shuang FENG, Yang HU, Wei-Xi YANG, Yue HAN1, Yi-Guang WANG*, and Li-Min GONG2*

Institute of Medicinal Biotechnology, CAMS and PUMC, Beijing 100050, China; 1Department of Pathophysiology, PLA General Hospital, Beijing 100853, China;
 
2Department of Cardiology, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

Abstract        The actin-myosin contractile apparatus consists of several thick filament and thin filament proteins. Specific regulatory mechanisms are involved in this highly ordered process. In this paper, we reported the identification and characterization of a novel myofibrillogenesis regulator, MR-1. The MR-1 gene was cloned from human skeletal muscle cDNA library by using a strategy that involves EST data base searching, PCR and RACE. The MR-1 gene is located on human chromosome 2q35 and encodes a 142 aa protein. Northern blot revealed that the mRNA level of MR-1 was highest in the skeletal muscle and certain level of MR-1 expression was also observed in heart, liver and kidney. Immunohistochemical assay confirmed that the MR-1 protein existed in human myocardial myofibrils. It was found by yeast two-hybrid screening and confirmed by in vitro binding assay that MR-1 could interact with sarcomeric proteins, such as myosin regulatory light chain, myomesin 1 and b-enolase. These studies suggested that MR-1 might play a regulatory role in the muscle cell and it was worth investigating further.

Key words        MR-1; gene cloning; heart; muscle; yeast two-hybrid

 

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Received: February 18, 2004       Accepted: April 18, 2004

This work was supported by a grant from the Beijing Major Project of Science and Technology (No. H020220020310)

*Corresponding authors:

Yi-Guang WANG: Tel, 86-10-63038137; Fax, 86-10-63038137; E-mail, [email protected]

Li-Min GONG: Tel, 001-713-5630412; Fax, 001-713-7451942; E-mail, [email protected]