Methyl Esterification of Cell Wall Constituents under the Influence of Auxin.

Abstract

IAA treatment of Avena coleoptile sections causes the methyl carbon of C14-labeled methyl methionine to be incorporated into the pectin ester of the cell wall more rapidly than is the case in the absence of IAA. The effect is detectable within 30 to 60 minutes. IAA has no apparent effect on incorporation of methyl carbon into protopectin ester. As the osmotic pressure external to the sections is increased, incorporation of methionine methyl into pectic esters decreases. The auxin induced increase in incorporation into pectin ester is, however, essentially unaffected up to external mannitol concentrations of 0.3 [image]. The antiauxin 2,4,6-T, given in the absence of added auxin, has no effect on methyl carbon incorporation into pectin ester but depressed incorporation into protopectin ester. Incorporation of methyl carbon into pectin apparently possesses a basal rate which is not auxin controlled. Both 2,4-DNP and argon treatment inhibit incorporation of methyl carbon into all cell wall fractions. This inhibition is apparent even when corrections are made for effects on the amount of substrate absorbed. The increased incorporation of glucose-C14 into pectin caused by auxin can be shown to be principally due to incorporation into saponifiable substituents, presumably methyl ester groups. The data support the hypothesis that esterification of carboxyl groups of pectin is involved in the auxin mechanism of cell expansion.