Targeted Modification of Homogalacturonan by Transgenic Expression of a Fungal Polygalacturonase Alters Plant Growth

Author:

Capodicasa Cristina1,Vairo Donatella1,Zabotina Olga1,McCartney Lesley1,Caprari Claudio1,Mattei Benedetta1,Manfredini Cinzia1,Aracri Benedetto1,Benen Jacques1,Knox J. Paul1,De Lorenzo Giulia1,Cervone Felice1

Affiliation:

1. Dipartimento di Biologia Vegetale e Laboratorio di Genomica Funzionale e Proteomica, Università di Roma La Sapienza, 00185 Rome, Italy (C.C., D.V., O.Z., C.C., B.M., C.M., B.A., G.D., F.C.); Centre for Plant Sciences, University of Leeds, Leeds, United Kingdom (L.M., J.P.K.); and Fungal Genomics Group, Laboratory for Microbiology, Agricultural University, NL–6703 HA Wageningen, The Netherlands (

Abstract

Abstract 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.

Publisher

Oxford University Press (OUP)

Subject

Plant Science,Genetics,Physiology

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