Atmungswege bei vernarbenden und proliferierenden Gewebefragmenten der Kartoffelknolle

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Abstract
The typical wound respiration drift (O2 und CO2) of 1 mm disks, which amounts to 6 times the values measured immediately after derepression, develops only if cicatrization takes place, but never in proliferating or non-proliferating tissues without suberin biosynthesis. The respiration rate of the latter is merely approximately doubled during the first 8 hours and maintains a steady state level continuously for 6 days. The respiratory drift is not affected by methods of tissue preparation and CO2-concentration per se but only depends on the induction or inhibition of suberin synthesis. Cyanide inhibition experiments evidently indicate an electron transfer mechanism by suberizing cells during the first 48 hours which is linked to cytochrome oxidase activity to a considerable extent, whereas proliferating tissue respiration nearly quantitatively follows a different pathway of cyanide-resistant terminal oxidation. Malonate inhibition experiments show the total respiration of proliferating tissue to be resistant, which therefore is bound to the activity of a pathway different from the tricarboxylic acid cycle. Predominantly the action of the pentose-phosphate-shunt must be responsible for energy producing processes and metabolism which finally regulate cell proliferation as well as cell division. Malonate sensitive respiration, that is TCA-cycle activity, is developed only in periderm-forming tissue. Its volume is shown to be in congruence with the amount of “induced respiration” evolved after 8 hours and is responsible for the typical maximum curve. In contrast the resistant basal level is in congruence with the total respiration volume of proliferating disks. The results indicate a direct relationship between increased TCA-cycle activity and suberin synthesis rather than a relationship between TCA-cycle and cellular processes such as protein synthesis, cell division or elongation, as emphasized by other authors.