Your browser doesn't support javascript.
loading
Montrer: 20 | 50 | 100
Résultats 1 - 2 de 2
Filtrer
Plus de filtres











Base de données
Gamme d'année
1.
Mol Plant Microbe Interact ; 26(1): 97-105, 2013 Jan.
Article de Anglais | MEDLINE | ID: mdl-22857385

RÉSUMÉ

Root-knot nematodes (RKN) are obligate biotrophic parasites that settle close to the vascular tissues in roots, where they induce the differentiation of specialized feeding cells and maintain a compatible interaction for 3 to 8 weeks. Transcriptome analyses of the plant response to parasitic infection have shown that plant defenses are strictly controlled during the interaction. This suggests that, similar to other pathogens, RKN secrete effectors that suppress host defenses. We show here that Mi-CRT, a calreticulin (CRT) secreted by the nematode into the apoplasm of infected tissues, plays an important role in infection success, because Mi-CRT knockdown by RNA interference affected the ability of the nematodes to infect plants. Stably transformed Arabidopsis thaliana plants producing the secreted form of Mi-CRT were more susceptible to nematode infection than wild-type plants. They were also more susceptible to infection with another root pathogen, the oomycete Phytophthora parasitica. Mi-CRT overexpression in A. thaliana suppressed the induction of defense marker genes and callose deposition after treatment with the pathogen-associated molecular pattern elf18. Our results show that Mi-CRT secreted in the apoplasm by the nematode has a role in the suppression of plant basal defenses during the interaction.


Sujet(s)
Arabidopsis/parasitologie , Calréticuline/métabolisme , Régulation de l'expression des gènes végétaux/génétique , Maladies des plantes/parasitologie , Tylenchoidea/pathogénicité , Animaux , Arabidopsis/génétique , Arabidopsis/immunologie , Arabidopsis/physiologie , Calréticuline/génétique , Prédisposition aux maladies , Femelle , Analyse de profil d'expression de gènes , Techniques de knock-down de gènes , Protéines d'helminthes/génétique , Protéines d'helminthes/métabolisme , Interactions hôte-parasite , Solanum lycopersicum/parasitologie , Numération des oeufs de parasites , Phytophthora/pathogénicité , Feuilles de plante/génétique , Feuilles de plante/parasitologie , Feuilles de plante/physiologie , Interférence par ARN , ARN des plantes/génétique , Plant/génétique , Plant/parasitologie , Plant/physiologie , Délétion de séquence , Nicotiana/parasitologie , Tylenchoidea/physiologie , Virulence
2.
Insect Mol Biol ; 19 Suppl 2: 229-39, 2010 Mar.
Article de Anglais | MEDLINE | ID: mdl-20482653

RÉSUMÉ

Phenotypic plasticity in response to environmental change is a common phenomenon, yet is poorly understood at the genetic and molecular level. Aphids exhibit a reproductive plasticity whereby seasonal changes result in asexual or sexual reproduction. To investigate the genetic basis of this reproductive plasticity, we assessed the meiosis and cell cycle gene repertoire in the genome of the pea aphid, Acyrthosiphon pisum. Aphids possess meiotic recombination genes and G1-to-S phase transition regulatory genes in gene copy numbers similar to other metazoans. However, mitotic and meiotic regulatory genes have duplicated, and several paralogues exhibit differential expression between reproductive morphs. Together, this suggests that cell cycle plasticity may be important in the evolution and mechanism of aphid reproductive plasticity.


Sujet(s)
Aphides/génétique , Gènes d'insecte , Séquence d'acides aminés , Animaux , Aphides/physiologie , Cycle cellulaire/génétique , Kinases cyclines-dépendantes/génétique , Évolution moléculaire , Femelle , Dosage génique , Duplication de gène , Génome d'insecte , Protéines d'insecte/génétique , Méiose/génétique , Mitose/génétique , Données de séquences moléculaires , Parthénogenèse/génétique , Parthénogenèse/physiologie , Pisum sativum/parasitologie , Phénotype , Phylogenèse , Reproduction asexuée/génétique , Reproduction asexuée/physiologie , Saisons , Spécificité d'espèce
SÉLECTION CITATIONS
DÉTAIL DE RECHERCHE