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Rheological analysis of viscoelastic cell wall changes in maize coleoptiles as affected by auxin and osmotic stress
Author(s) -
Hohl Michael,
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.tb00960.x
Subject(s) - turgor pressure , coleoptile , cell wall , auxin , biophysics , elongation , viscoelasticity , osmotic pressure , osmotic shock , chemistry , materials science , biology , biochemistry , composite material , ultimate tensile strength , gene
The effects of auxin and osmotic stress on elongation growth of maize ( Zea mays L.) coleoptile segments are accompanied by characteristic changes in the extensibility of the growth‐limiting cell walls. At full turgor auxin causes growth by an increase in wall extensibility (wall looseining). Growth can be stopped by an osmotically produced step‐down in turgor of 0.45 MPa. Under these conditions auxin causes the accumulation of a potential for future wall extension which is released after restoration of full turgor. Turgor reduction causes a reversible decrease in wall extensibility (wall stiffening) both in the presence and absence of auxin. These changes in vivo are correlated with corresponding changes in the rheological properties of the cell walls in vitro which can be traced back to specific modifications in the shape of the hysteretic stress‐strain relationship. The longitudinally load‐bearing walls of the coleoptile demonstrate almost perfect viscoelasticity as documented by a nearly closed hysteresis loop. Auxin‐mediated wall loosening causes an increase of loop width and thus affects primarily the amount of hysteresis in the isolated wall. In contrast, turgor reduction by osmotic stress reduces loop length and thus affects primarily the amount of viscoelastic wall extensibility. Pretreatment of segments with anoxia and H 2 O 2 modify the hysteresis loop in agreement with the conclusion that the wall‐stiffening reaction visualized under osmotic stress in vivo is an O 2 ‐dependent process in which O 2 can be substituted by H 2 O 2 . Cycloheximide specifically inhibits auxin‐mediated wall loosening without affecting wall stiffening, and this is mirrored in specific changes of the hysteresis loop. Corroborating a previous in vivo study (Hohl et al. 1995, Physiol. Plant. 94: 491–498) these results show that cell wall stiffening in vivo can also be demonstrated by Theological measurements with the isolated cell wall and that this process can be separated from cell wall loosening by specific changes in the shape of the hysteresis loop.