Detailed Information |
You are checking out the detail information about this geneset. |
| Standard Gene Set Name | WILLIAM_LFY_UP |
| Species | Arabidopsis thaliana |
| Brief Description | Induced directly-14 genes are good candiDates for direct targets of LFY because they are induced directly (without protein synthesis) after LFY ctivation and are expressed at elevated levels in plants that constitutively overexpress LFY (Table 1 PubmedID:14736918) |
| Full Description/Abstract | The switch from vegetative to reproductive development in plants necessitates a switch in the developmental program of the descendents of the stem cells in the shoot apical meristem. Genetic and molecular investigations have demonstrated that the plant-specific transcription factor and meristem identity regulator LEAFY (LFY) controls this developmental transition by inducing expression of a second transcription factor, APETALA1, and by regulating the expression of additional, as yet unknown, genes. Here we show that the additional LFY targets include the APETALA1-related factor, CAULI-FLOWER, as well as three transcription factors and two putative signal transduction pathway components. These genes are up-regulated by LFY even when protein synthesis is inhibited and, hence, appear to be direct targets of LFY. Supporting this conclusion, cis-regulatory regions upstream of these genes are bound by LFY in vivo. The newly identified LFY targets likely initiate the transcriptional changes that are required for the switch from vegetative to reproductive development in Arabidopsis. The plant-specific LEAFY (LFY) protein is necessary and sufficient for the vital switch from vegetative to reproductive development in dicotyledonous plant species (1-9). LFY controls the production of the flowers, which are formed in lieu of secondary inflorescences from the flanks of the shoot apical meristem. Because LFY is required for all of the major features that differentiate flowers from inflorescence branches, it is referred to as a meristem identity gene. After initiating the meristem identity switch, LFY has a second role in the activation of the floral homeotic genes that specify the identity of organs in the flower (10). The two roles of LFY are separable genetically and molecularly (11, 12). LFY exerts its developmental effects by means of transcriptional regulation; LFY has been shown to be a transcription factor in vivo (13, 14). Despite the critical importance of this regulator, only three direct targets of LFY have been identified (13-15). Two of the targets, AGAMOUS and APETALA3, are floral homeotic genes that act directly downstream of LFY in flower morphogenesis. Only one known direct LFY target gene product, APETALA1 (AP1), acts in the meristem identity pathway (13). The ap1-1 mutation partly suppresses the LFY gain-of-function phenotype (9, 16), indicating that AP1 acts downstream of LFY in the floral transition, which culminates in flower formation. Posttranslational activation of a biologically active fusion protein between LFY and the rat glucocorticoid receptor (GR) hormone-binding domain demonstrates that LFY directly activates AP1 in the anlagen of the flower primordia in a protein synthesis-independent fashion (13). In addition, LFY binds to cis-regulatory elements that control AP1 expression (11). Thus, LFY regulates the transition to flower development, at least in part, by inducing AP1 expression in regions of the shoot apical meristem that give rise to flower primordia. LFY null mutations cause striking defects in the transition to reproductive development; lfy-6 plants, for example, produce a large number of secondary inflorescences until very late in development when defective flowers are formed (1-3). In contrast, the strongest available AP1 mutation has a much weaker effect on inflorescence morphology, implying that other LFY target genes must exist in the meristem identity pathway. AP1 acts as a floral homeotic gene in addition to its role as a meristem identity regulator (17, 18). The latter function does not depend on LFY, however, because lfy null mutants show strong AP1 expression in flowers from stage three onward (11, 13, 16, 19). The LFY-independent induction of AP1 expression makes it difficult to detect LFY-dependent induction of AP1 at the floral transition by using quantitative methods in entire inflorescences (13). To identify the additional unknown LFY targets that act at the transition to reproductive development together with AP1, it is, therefore, important to first identify a developmental stage at which quantitative induction of AP1 can be observed in response to LFY. Here we report that quantitative up-regulation of AP1 can be readily observed in 9-day-old seedlings. Using posttranslational activation of LFY-GR, we demonstrate that the closest AP1 homolog, CAULIFLOWER (CAL), is a direct LFY target at this stage in development and that cis-regulatory elements in the putative CAL promoter are bound by LFY. We used microarray analysis to identify direct targets of LFY and chromatin immunoprecipitation (ChIP) to demonstrate in vivo LFY binding to the putative promoter regions of these genes. The predicted function of the proteins encoded by these genes is consistent with their role in the meristem identity switch |
| External Pathway ID/Pubmed ID | 14736918 |
| Source | Literature |
| Contributor/Author | Liming Lai and Xijin Ge |
| Organization of contributer | South Dakota State University |
| External URL | http://www.pnas.org/content/101/6/1775.full.pdf+html |