1,721,271 research outputs found
Normalization of GUS by luciferase activity from the same cell extract reduces transformation variability
No full textPolygalacturonase-inhibiting proteins in defense against phytopathogenic fungi
No full textPolygalacturonase-inhibiting proteins (PGIPs) are ubiquitous plant cell wall proteins that are directed against fungal polygalacturonases (PGs), which are important pathogenicity factors. The inhibiting activity of PGIPs directly reduces the aggressive potential of PGs. In addition, it causes PGs to form more long-chain oligogalacturonides that are able to induce defense responses, thereby indirectly contributing to the plant defense. Recent evidence demonstrates that PGIPs are efficient defense proteins and limit fungal invasion. PGIPs and the products of many plant resistance genes share a leucine-rich repeat (LRR) structure, which provides specific recognition of pathogen-derived molecules. The high level of polymorphism of both PGIPs and polygalacturonases is an invaluable tool for deciphering the structure, function and evolution of plant LRR proteins and their ligands. Furthermore, information about PGIP structure and evolution paves the way to the development of efficient strategies for crop protection
Pectic enzymes as phytotoxins: absorption of polygalacturonase from Colletotrichum lindemuthianum to French bean protoplasts
No full textPolygalacturonase-Inhibiting Proteins (PGIPs): Their Role in Specificity and Defence against Pathogenic Fungi.
No full textThe role of polygalacturonase-inhibiting proteins (PGIPs) in defense against pathogenic fungi
No full textNucleotide sequence coding for a leucine-rich repeat receptor-like protein kinase (LRPKm1)
No full textIsolation and characterization of pectin-inducible cDNA clones from the phytopathogenic fungus Fusarium moniliforme
No full text
Oligogalacturonides inhibit the induction of late but not of early auxin-repressive genes in tobacco
No full textOligogalacturonides (OGs) released from the
plant cell wall regulate several defense responses, as well
as various aspects of plant growth and development. In
these latter effects, OGs exhibit auxin-antagonist activity.
To shed light on the mechanism by which OGs antagonise
auxin, we analysed the ability of these
oligosaccharides to inhibit the activityof four auxin-upregulated
promoters [pGm-GH3 of soybean (Glycine
max L. Merr.), pNt114 of tobacco (Nicotiana tabacum
L.), and prolB and prolD of Agrobacterium rhizogenes]
driving the expression of the b-glucuronidase reporter
gene (GUS) in transgenic tobacco seedlings. Our results
indicate that OGs at submicromolar concentrations inhibit
the activation byau xin of pNt114, prolB and
prolD, but not that of pGm-GH3. Comparative analysis
of the kinetics of activation of the four promoters in
response to the hormone shows that, while pGm-GH3 is
rapidlyactivat ed, the other three promoters exhibit a
delayed activation, with a lag of at least 4 h before the
appearance of GUS activity. The lack of effect of the
OGs on earlyau xin-responsive genes was confirmed by
RNA gel blot analysis of the tobacco genes Nt-GH3 and
Nt-iaa2.3/2.5. Our results suggest that the auxin-antagonist
action of OGs affects the expression of late but not
of early au xin-responsive genes
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