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The cryptic‐growth response of maize coleoptiles and its relationship to H 2 O 2 ‐dependent cell wall stiffening
Author(s) -
Hohl Michael,
Greiner Heribert,
Schopfer Peter
Publication year - 1995
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.1995.tb00959.x
Subject(s) - coleoptile , turgor pressure , cell wall , elongation , biophysics , peroxidase , stiffening , auxin , biology , chemistry , biochemistry , ultimate tensile strength , enzyme , materials science , gene , metallurgy , composite material
Auxin‐mediated elongation growth of maize ( Zea mays L.) coleoptile segments can be nullified by lowering the turgor pressure by 0.45 MPa. Under these conditions irreversible segment length (l in ) measured after freezing/thawing increases steadily over a period of 8 h although the in vivo length (l tot ) remains constant. This phenomenon, designated as ‘cryptic growth’, is an indication of a wall‐stiffening process which appears to be an intrinsic component of irreversible cell wall extension. Using a range of metabolic inhibitors it is demonstrated that cryptic growth is caused by a temperature‐sensitive biochemical process in the cell wall which depends on the presence of O 2 and active peroxidase, but not on ATP and protein synthesis. Inhibition of cryptic growth by anaerobic conditions can be alleviated by extermal H 2 O 2 . Moreover, cryptic growth can be partially inhibited by the antioxidant ascorbate. It is concluded that cryptic growth represents a wall‐stiffening reaction mediated by peroxidase‐catalyzed, H 2 O 2 ‐dependent cross‐linking of phenolic residues of wall polymers. The experimental demonstration of a wall‐stiffening reaction in a rapidly growing organ supports the concept that irreversible cell elongation (growth) is caused by an interplay of two chemorheological reactions, a turgor‐dependent wall‐loosening reaction and a separate wall‐stiffening reaction which fixes the viscoelastically extended wall structure through oxidative cross‐linking and thus conferring irreversibility to wall extension.