Targeted Modification of Homogalacturonan by Transgenic Expression of a Fungal Polygalacturonase Alters Plant Growth
Author(s) -
Cristina Capodicasa,
Donatella Vairo,
Olga A. Zabotina,
Lesley McCartney,
Claudio Caprari,
Benedetta Mattei,
Cinzia Manfredini,
B. Aracri,
Jacques Benen,
John Knox,
Giulia De Lorenzo,
Felice Cervone
Publication year - 2004
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.104.042788
Subject(s) - nicotiana tabacum , arabidopsis , mutant , transgene , pectinase , biology , cell wall , aspergillus niger , mutagenesis , arabidopsis thaliana , transformation (genetics) , wild type , genetically modified crops , biochemistry , gene , enzyme
Pectins are a highly complex family of cell wall polysaccharides comprised of homogalacturonan (HGA), rhamnogalacturonan I and rhamnogalacturonan II. We have specifically modified HGA in both tobacco (Nicotiana tabacum) and Arabidopsis by expressing the endopolygalacturonase II of Aspergillus niger (AnPGII). Cell walls of transgenic tobacco plants showed a 25% reduction in GalUA content as compared with the wild type and a reduced content of deesterified HGA as detected by antibody labeling. Neutral sugars remained unchanged apart from a slight increase of Rha, Ara, and Gal. Both transgenic tobacco and Arabidopsis were dwarfed, indicating that unesterified HGA is a critical factor for plant cell growth. The dwarf phenotypes were associated with AnPGII activity as demonstrated by the observation that the mutant phenotype of tobacco was completely reverted by crossing the dwarfed plants with plants expressing PGIP2, a strong inhibitor of AnPGII. The mutant phenotype in Arabidopsis did not appear when transformation was performed with a gene encoding AnPGII inactivated by site directed mutagenesis.
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