The brevipedicellus (bp) mutant, caused by a loss-of-function mutation in the KNAT1 homeobox gene, is known to affect the stem morphogenesis. BP and ERECTA (ER) genes are required to promote internode and pedicel development and delineate nodal boundaries to maintain the radial symmetry of stems and pedicels. My research aims to identify genes acting on the BP pathway by utilizing a forward genetics approach. The suppressor4 mutant, identified from the bp er mutant screen, exhibits moderate length and perpendicularly-oriented pedicels with partially formed distal pedicel bulges, absent in the bp mutant. The kinky mutant, identified from the bp mutant screen, develops severe bends at the floral nodes and enhanced achlorophyllous stripes. These results suggest the SUPPRESSOR4 gene contribution in inhibiting the development of distal pedicel bulge and influencing both pedicel angle and length whereas the KINKY gene might act with BP in regulating proper inflorescence development.

In Arabidopsis, the F-box gene family encodes a large number of proteins postulated to act as substrate selectors for proteasome-mediated protein degradation. Recent reports document the importance of F-box proteins in developmental and metabolic signaling. Our microarray analyses of inflorescences of the brevipedicellus(bp) mutant indicate several F-box proteins are upregulated, suggesting that BP represses these genes in wild type plants to condition normal inflorescence development. We undertook analyses to examine the function of these proteins and their contribution to the pleiotropic phenotypes of bp. Yeast-2-hybrid screens revealed that the F-box protein At1g80440 binds to phenylalanine ammonia lyase-1(PAL1), the gateway enzyme of phenylpropanoid metabolism. Transgenic lines driven by the 35S cauliflower mosaic virus were attained but could not be propagated, suggesting a fatal phenotype. BP driven F-box expression results in phyllotaxy defects, manifest as alterations in the emergence of inflorescence and floral meristems in the axils of some cauline leaves.

In Arabidopsis, the F-box gene family encodes a large number of proteins postulated to act as substrate selectors for proteasome-mediated protein degradation. Recent reports document the importance of F-box proteins in developmental and metabolic signaling. Our microarray analyses of inflorescences of the brevipedicellus(bp) mutant indicate several F-box proteins are upregulated, suggesting that BP represses these genes in wild type plants to condition normal inflorescence development. We undertook analyses to examine the function of these proteins and their contribution to the pleiotropic phenotypes of bp. Yeast-2-hybrid screens revealed that the F-box protein At1g80440 binds to phenylalanine ammonia lyase-1(PAL1), the gateway enzyme of phenylpropanoid metabolism. Transgenic lines driven by the 35S cauliflower mosaic virus were attained but could not be propagated, suggesting a fatal phenotype. BP driven F-box expression results in phyllotaxy defects, manifest as alterations in the emergence of inflorescence and floral meristems in the axils of some cauline leaves.

The brevipedicellus (bp) mutant, caused by a loss-of-function mutation in the KNAT1 homeobox gene, is known to affect the stem morphogenesis. BP and ERECTA (ER) genes are required to promote internode and pedicel development and delineate nodal boundaries to maintain the radial symmetry of stems and pedicels. My research aims to identify genes acting on the BP pathway by utilizing a forward genetics approach. The suppressor4 mutant, identified from the bp er mutant screen, exhibits moderate length and perpendicularly-oriented pedicels with partially formed distal pedicel bulges, absent in the bp mutant. The kinky mutant, identified from the bp mutant screen, develops severe bends at the floral nodes and enhanced achlorophyllous stripes. These results suggest the SUPPRESSOR4 gene contribution in inhibiting the development of distal pedicel bulge and influencing both pedicel angle and length whereas the KINKY gene might act with BP in regulating proper inflorescence development.

Notre équipe de recherche étudie l'action des hormones gibbérellines (GA) et cytokinines (CK) dans les processus de développement chez la plante modèle Arabidopsis thaliana. En recherchant des régulateurs de l'expression d'un gène impliqué dans la différenciation des cellules épidermiques et dont l'expression est contrôlée par ces deux hormones, une nouvelle famille de quatre protéines nommées GeBP (GL1 enhancer Binding Protein), GPL1 (GeBP Protein Like 1), GPL2 et GPL3 a été identifiée au laboratoire. Le but de ce travail de thèse était de caractériser moléculairement et fonctionnellement les membres de cette nouvelle famille multigénique.<br /> Nous avons tout d'abord vérifié l'adressage nucléaire des protéines GeBP/GPL et démontré leur capacité à former des dimères in planta via un motif Leucine-Zipper non canonique. L'analyse fonctionnelle a été abordée par l'étude de lignées simples et multiples mutantes gebp/gpl. Différentes données physiologiques et moléculaires convergentes ont démontré un rôle redondant des gènes GeBP/GPL dans le contrôle de la réponse aux CK. Enfin, une analyse globale des transcriptomes d'une lignée surexpresseur de GPL2 et du quadruple mutant gebp/gpl, nous a permis d'établir un lien entre les GeBP/GPL et CPR5, un gène impliqué dans la réponse aux pathogènes, et le contrôle du cycle cellulaire. Ce lien a été conforté expérimentalement par des mesures de ploïdies des noyaux des cellules foliaires montrant une dérégulation du cycle cellulaire chez la lignée quadruple mutant et la lignée surexpresseur de GPL2.<br />Les futurs travaux auront pour but de poursuivre l'étude de la fonction des GeBP/GPL et de confirmer le lien avec CPR5.