Abstract

Pectin metabolism was analyzed in tabasco pepper (Capsicum frutescens L.) to determine the metabolic process associated with the ease of fruit detachment from the calyx. Two genotypes that differ in the fruit detachment force (FDF) were used: 'Easy Pick' (EZ) which requires a low force and 'Hard Pick' (HP) which requires higher force. Pectin dissolution in fresh ripe fruit tissue and in extracted fruit cell wall was higher in the EZ genotype than the HP genotype and inversely correlated to the FDF. Size-exclusion chromatography of EDTA-soluble polyuronides indicated that pectin was degraded in ripe tissue from both genotypes, but the degree of depolymerization was more extensive in the EZ genotype. The ease of fruit detachment was, therefore, attributed to pectin ultra-degradation. Polygalacturonase activity, however, was the same in protein extracts from both genotypes. In contrast, pectin methyl-esterase (PME) activity in vivo assessed by methanol production was detected in ripe fruit of the EZ genotype only and it was associated with the FDF decline. The decrease in degree of pectin esterification and pH at the fruit junction area detected in EZ ripe fruit was attributed to PME activity in vivo. PME activity in vitro, however, was detected in protein extracts and disrupted tissue from both genotypes at all ripening stages. This suggests that a PME regulatory mechanism may be blocking PME activity in vivo. Two PME isoforms were detected in protein extracts from ripe fruit. The PME-1 form was detected in EZ genotype only and appears to be responsible for methanol production in vivo. A predominant 36.7 k protein was associated with localized pH reduction in a pectin-agarose gel. The PME-2 form was detected in both genotypes and appears to be active in disrupted tissue only. A 40.8 k protein was resolved consistently in PME-2 active fractions. In conclusion, PME-1 appears to be responsible for PME activity in vivo and was associated with the ease of fruit detachment in tabasco pepper.

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