Investigation of hyaluronan function in the mouse through targeted mutagenesis

It has become increasingly apparent that the high molecular mass glycosaminoglycan, hyaluronan (HA), is required for many morphogenetic processes during vertebrate development. This renewed understanding of the various developmental roles for HA, has come about largely through the advent of gene tar...

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Bibliographic Details
Published in:Glycoconjugate journal 2002-05, Vol.19 (4-5), p.341-345
Main Authors: Spicer, Andrew P, Tien, Janet Lee, Joo, Adriane, Bowling, Jr, Rodney A
Format: Article
Language:English
Subjects:
Animals
Biosynthesis
Gene Expression Regulation, Developmental
Gene Expression Regulation, Enzymologic
Gene Targeting - methods
Genes
Glucuronosyltransferase - deficiency
Glucuronosyltransferase - genetics
Glucuronosyltransferase - physiology
Hyaluronan Synthases
Hyaluronic Acid - deficiency
Hyaluronic Acid - genetics
Hyaluronic Acid - physiology
Mice
Mice, Knockout
Mutagenesis
Phenotype
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Summary:It has become increasingly apparent that the high molecular mass glycosaminoglycan, hyaluronan (HA), is required for many morphogenetic processes during vertebrate development. This renewed understanding of the various developmental roles for HA, has come about largely through the advent of gene targeting approaches in the mouse. To date, mutations have been engineered in the enzymes responsible for biosynthesis and degradation and for those proteins that bind to HA within the extracellular matrix and at the cell surface. Collectively, the phenotypes resulting from these mutations demonstrate that HA is critical for normal mammalian embryogenesis and for various processes in postnatal and adult life (Table 1). In this article we will review our progress in understanding the biological functions for HA through targeted mutagenesis of the HA synthase 2 (Has2) and 3 (Has3) genes. Data that has been obtained from a conventional targeted disruption of the Has2 gene, is presented in an accompanying review by Camenisch and McDonald. More specifically, in this review we will provide an overview of the conditional gene targeting strategy being used to create tissue-specific deficiencies in Has2 function, along with our progress in understanding the role for Has3-dependent HA biosynthesis.
ISSN:0282-0080
1573-4986
DOI:10.1023/a:1025321105691