Maturation of potato (Solanum tuberosum L.) tuber native and
wound periderm and development of resistance to periderm abrasion were investigated utilizing cytological and histochemical techniques. Both native and
wound periderm consist of three different tissues: phellem, phellogen and phelloderm. It was previously determined that the phellogen walls of immature native periderm are thin and prone to fracture during harvest, leading to periderm abrasion (excoriation). Phellogen walls thicken and become less susceptible to fracture upon maturation of the periderm, leading to resistance to excoriation. We now demonstrate that phellogen cells of immature
wound periderm also have thin radial walls and that
wound periderm abrasion is due to fracture of these walls. Maturation of the
wound periderm is also associated with an increase in the thickness of the phellogen radial walls. Histological analysis with
ruthenium red and hydroxylamine-FeCI2, which
stain unesterified and highly methyl-esterified
pectins, respectively, indicates that the phellogen cell walls of native and
wound periderm differ significantly regardless of the stage of maturity. Results obtained by staining with
ruthenium red and hydroxylamine-FeCI2 imply that phellogen cell walls of immature native periderm contain methyl-esterified
pectin, but are lacking in unesterified (acidic)
pectins. Maturation of native periderm is accompanied by an apparent increase in unesterified
pectins in the walls of phellogen cells, which may allow for the strengthening of phellogen cell walls via
calcium pectate formation. Histological staining of the phellogen walls of
wound periderm, on the other hand, implies that these walls are deficient in
pectins. Moreover, maturation of
wound periderm is not accompanied by an increase in unesterified
pectins in these walls. Since
peroxidase is known to catalyse the cross-linking of cell wall
polymers, we stained native and
wound periderm for the presence of
peroxidase utilizing
guaiacol as a substrate.
Peroxidase staining was strong in the phellogen walls of both immature and mature native periderm and we could not detect any differences in staining between them.
Peroxidase staining was weak in the phellogen walls of immature
wound periderm and was not detectably different in mature
wound periderm.
Peroxidase data imply that there are distinct differences between native and
wound periderm, though our data do not indicate that changes in
peroxidase activity are involved in the development of resistance to periderm abrasion that occurs upon maturation of the periderm. However, we cannot rule out the involvement in this process of
peroxidase isozymes that have low affinity for the substrates utilized here.