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It has been shown in an earlier communication (11) that auxin increases the amount of incorporation of carbon-14 derived from methyl labeled methionine into a fraction of the cell wall of Avena coleoptile sections which possesses the properties classically associated with pectin. Incorporation into this material represents but a small part of the total, the main part being into the protopectin fraction. Such incorporation is not significantly affected by the presence of auxin. The auxin effect on incorporation into the pectin fraction persists in solutions which contain sufficient mannitol to prevent elongation during the course of the experiment. C14 from glucose was also found to be incorporated into pectin more rapidly under the influence of auxin. Bennet-Clark (1) and others have also suggested that auxin causes an increase in the methyl content of pectic substances of cell walls of elongating tissue. The hypothesis may be formulated that methylation of the carboxyl groups of adjacent pectin molecules under the influence of auxin may be involved in the splitting of anhydride or calcium bridges which contribute to the mechanical properties of the cell wall. The present investigation was undertaken to determine to what extent general metabolic inhibitors interfere with the incorporation of methionine methyl into the pectin fraction and to answer definitively the question of whether methyl carbon incorporation accompanies only net pectin synthesis or whether such incorporation occurs at a more rapid rate than net synthesis and is therefore to be regarded as methyl ester turnover. It will also be shown below that esterification of pectin by methyl derived carbon is an auxin controlled reaction.

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