Cell Wall Metabolism

Abstract

INTRODUCTION The cell wall is dead? The cell wall is alive and well? The cell wall consists of an amorphous hemicellulose pectin matrix in which lie cellulose micro­ fibrils? The cell wall consists of a highly ordered macromolecular multi­ l ayered network? Does the cell wall age? How are cell wall components synthesized? Where is the site of bio­ synthesis? Are Golgi, plasma membrane, endoplasmic reticulum, or micro­ tubules involved? How are the components transferred and inserted into the wall structure? Why are the growing ends of cellulose microfibrils not ob­ served? What mechanisms control the changeover from primary wall to secondary wall biosynthesis? What is the explanation for the great difference between the degree of polymerization of primary wall and secondary wall cellulose? Is the Loewus pathway for inositol metabolism of significance in changes from primary to secondary wall formation? What is the role of cell wall enzymes such as ascorbic acid oxidase, peroxidase, invertase, phospha­ tase, etc? Which of the multitude of possible cross-linkages actually exist in the wall, and which, if any of these, are labile and under cellular control? I f cell wall autolysis is involved in cell wall growth, which enzymes (autolysins?) are involved? How is the turnover of cell wall components related to growth? What is the role of the hydroxyproline-rich cell wall pro­ tein extensin ? What proportion of the wall polysaccharide is attached to the wall glycoprotein? Is there a protein glycan network in any way analo­ gous to bacterial peptido-glycan? Is it possible to show localization of hy­ droxyproline-rich protein by autoradiography? (Why have different workers reached different conclusions?) Is it meaningful to use such cl assical terms as apposition and intussusception in considering how cell walls grow? Are classical terms such as pectic substances and hemicellulose sufficiently pre-