Beyond the divide: Boundaries for patterning and stem cell regulation in plants

The initiation of plant lateral organs from the shoot apical meristem (SAM) is closely associated with the formation of specialized domains of restricted growth known as the boundaries. These zones are required in separating the meristem from the growing primordia or adjacent organs but play a much broader role in regulating stem cell activity and shoot patterning. Studies have revealed a network of genes and hormone pathways that establish and maintain boundaries between the SAM and leaves. Recruitment of these pathways is shown to underlie a variety of processes during the reproductive phase including axillary meristems production, flower patterning, fruit development, and organ abscission. This review summarizes the role of conserved gene modules in patterning boundaries throughout the life cycle

Analyse fonctionnelle du gène à homéoboîte KNAT2 d'Arabidopsis thaliana

PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Combinations of mutations sufficient to alter Arabidopsis leaf dissection

Leaves show a wide range of shapes that results from the combinatory variations of two main parameters: the relative duration of the morphogenetic phase and the pattern of dissection of the leaf margin. To further understand the mechanisms controlling leaf shape, we have studied the interactions between several loci leading to increased dissection of the Arabidopsis leaf margins. Thus, we have used (i) mutants in which miR164 regulation of the CUC2 gene is impaired, (ii) plants overexpressing miR319/miRJAW that down-regulates multiple TCP genes and (iii) plants overexpressing the STIMPY/WOX9 gene. Through the analysis of their effects on leaf shape and KNOX I gene expression, we show that these loci act in different pathways. We show, in particular, that they have synergetic effects and that plants combining two or three of these loci show dramatic modifications of their leaf shapes. Finally, we present a working model for the role of these loci during leaf development

Interaction of KNAT6 and KNAT2 with BREVIPEDICELLUS and PENNYWISE in Arabidopsis Inflorescences[W]

The three amino acid loop extension (TALE) homeodomain superfamily, which comprises the KNOTTED-like and BEL1-like families, plays a critical role in regulating meristem activity. We previously demonstrated a function for KNAT6 (for KNOTTED-like from Arabidopsis thaliana 6) in shoot apical meristem and boundary maintenance during embryogenesis. KNAT2, the gene most closely related to KNAT6, does not play such a role. To investigate the contribution of KNAT6 and KNAT2 to inflorescence development, we examined their interactions with two TALE genes that regulate internode patterning, BREVIPEDICELLUS (BP) and PENNYWISE (PNY). Our data revealed distinct and overlapping interactions of KNAT6 and KNAT2 during inflorescence development. Removal of KNAT6 activity suppressed the pny phenotype and partially rescued the bp phenotype. Removal of KNAT2 activity had an effect only in the absence of both BP and KNAT6 or in the absence of both BP and PNY. Consistent with this, KNAT6 and KNAT2 expression patterns were enlarged in both bp and pny mutants. Thus, the defects seen in pny and bp are attributable mainly to the misexpression of KNAT6 and to a lesser extent of KNAT2. Hence, our data showed that BP and PNY restrict KNAT6 and KNAT2 expression to promote correct inflorescence development. This interaction was also revealed in the carpel

KNAT6: An Arabidopsis Homeobox Gene Involved in Meristem Activity and Organ Separation

The homeobox gene family plays a crucial role during the development of multicellular organisms. The KNOTTED-like genes from Arabidopsis thaliana (KNAT6 and KNAT2) are close relatives of the meristematic genes SHOOT MERISTEMLESS (STM) and BREVIPEDICELLUS, but their function is not currently known. To investigate their role, we identified null alleles of KNAT6 and KNAT2. We demonstrate that KNAT6 contributes redundantly with STM to the maintenance of the shoot apical meristem (SAM) and organ separation. Consistent with this role, the expression domain of KNAT6 in the SAM marks the boundaries between the SAM and cotyledons. The lack of meristematic activity in the knat6 stm-2 double mutant and the fusion of cotyledons were linked to the modulation of CUP-SHAPED COTYLEDON (CUC) activity. During embryogenesis, KNAT6 is expressed later than STM and CUC. In agreement with this fact, CUC1 and CUC2 were redundantly required for KNAT6 expression. These data provide the basis for a model in which KNAT6 contributes to SAM maintenance and boundary establishment in the embryo via the STM/CUC pathway. KNAT2, although the closest related member of the family to KNAT6, did not have such a function

The Homologous ABI5 and EEL Transcription Factors Function Antagonistically to Fine-Tune Gene Expression during Late Embryogenesis

In Arabidopsis, the basic leucine zipper transcription factor ABI5 activates several late embryogenesis–abundant genes, including AtEm1 and AtEm6. However, the expression of many other seed maturation genes is independent of ABI5. We investigated the possibility that ABI5 homologs also participate in the regulation of gene expression during seed maturation. We identified 13 ABI5-related genes in the Arabidopsis genomic sequence. RNA gel blot analysis showed that seven of these genes are active during seed maturation and that they display distinct expression kinetics. We isolated and characterized two mutant alleles of one of these genes, AtbZIP12/EEL. Unlike abi5, the eel mutations did not inhibit the expression of any of the maturation marker genes that we monitored. On the contrary, the accumulation of the AtEm1 and AtEm6 mRNAs was enhanced in eel mutant seeds compared with wild-type seeds. Gel mobility shift assays, combined with analysis of the genetic interactions among the eel and abi5 mutations, indicated that ABI5 and EEL compete for the same binding sites within the AtEm1 promoter. This study illustrates how two homologous transcription factors can play antagonistic roles to fine-tune gene expression