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Molecular and Cellular Biology, November 1999, p. 7841-7845, Vol. 19, No. 11
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Normal Skeletal Development of Mice Lacking Matrilin 1: Redundant Function of Matrilins in Cartilage?

Attila Aszódi,1,* John F. Bateman,1,dagger Emilio Hirsch,2 Mária Baranyi,3 Ernst B. Hunziker,4 Nik Hauser,5 Zsuzsa Bösze,3 and Reinhard Fässler1

Department of Experimental Pathology, Lund University, 221 85 Lund, Sweden1; Department of Genetics, Biology and Biochemistry, University of Torino, 10126 Torino, Italy2; Agricultural Biotechnology Center, 2100 Gödöllö, Hungary3; and M.E. Müller Institute for Biomechanics, University of Bern, 3010 Bern,4 and Department of Rheumatology, University Hospital Zürich, 8091 Zürich,5 Switzerland

Received 22 July 1999/Accepted 3 August 1999

Matrilin 1, or cartilage matrix protein, is a member of a novel family of extracellular matrix proteins. To date, four members of the family have been identified, but their biological role is unknown. Matrilin 1 and matrilin 3 are expressed in cartilage, while matrilin 2 and matrilin 4 are present in many tissues. Here we describe the generation and analysis of mice carrying a null mutation in the Crtm gene encoding matrilin 1. Anatomical and histological studies demonstrated normal development of homozygous mutant mice. Northern blot and biochemical analyses show no compensatory up-regulation of matrilin 2 or 3 in the cartilage of knockout mice. Although matrilin 1 interacts with the collagen II and aggrecan networks of cartilage, suggesting that it may play a role in cartilage tissue organization, studies of collagen extractability indicated that collagen fibril maturation and covalent cross-linking were unaffected by the absence of matrilin 1. Ultrastructural analysis did not reveal any abnormalities of matrix organization. These data suggest that matrilin 1 is not critically required for cartilage structure and function and that matrilin 1 and matrilin 3 may have functionally redundant roles.

* Corresponding author. Mailing address: Department of Experimental Pathology, Lund University, S-22185 Lund, Sweden. Phone: 46-46-173-553. Fax: 46-46-158-202. E-mail: attila.aszodi{at}pat.lu.se.

dagger Present address: Department of Paediatrics, University of Melbourne, Royal Children's Hospital, Parkville VIC 3052, Australia.

Molecular and Cellular Biology, November 1999, p. 7841-7845, Vol. 19, No. 11
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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