Characterization of a ubiquitous expressed gene family encoding polygalacturonase in Arabidopsis thaliana

Citation
M. Torki et al., Characterization of a ubiquitous expressed gene family encoding polygalacturonase in Arabidopsis thaliana, GENE, 242(1-2), 2000, pp. 427-436
Citations number
28
Categorie Soggetti
Molecular Biology & Genetics
Journal title
GENE
ISSN journal
03781119 → ACNP
Volume
242
Issue
1-2
Year of publication
2000
Pages
427 - 436
Database
ISI
SICI code
0378-1119(20000125)242:1-2<427:COAUEG>2.0.ZU;2-2
Abstract
Pectin, as one of the major components of plant cell wall, has been implica ted in many developmental processes occurring during plant growth. Among th e different enzymes known to participate in the pectin structure modificati ons, polygalacturonase (PG) activity has been shown to be associated with f ruit ripening, organ abscission and pollen grain development. Until now, se quence analyses of the deduced polypeptides of the plant PG genes allowed t heir grouping into three clades corresponding to genes involved in one of t hese three activities. In this study, we report the sequence of three genom ic clones encoding PG in Arabidopsis thaliana. These genes, together with 1 6 other genes present in the databases form a large gene family, ubiquitous ly expressed. present on the five chromosomes with at least two gene cluste rs on chromosomes II and V, respectively. Phylogenetic analyses suggest tha t the A. thaliana gene family contains five classes of genes, with three of them corresponding to the previously defined clades. Comparison of positio ns and numbers of introns among the A. thaliana genes reveals structural co nservation between genes belonging to the same class. The pattern of intron losses that could have given rise to the PG gene family is consistent with a mechanism of intron loss by replacement of an ancestral intron-containin g gene with a reverse-transcribed DNA copy of a spliced mRNA. Following thi s event of intron loss, the acquisition of introns in novel positions is co nsistent with a mechanism of intron gain at proto-splice sites. (C) 2000 El sevier Science B.V. All rights reserved.