RESUMO
In seasonal flowering, plants need to monitor environmental variables. A combination of photoreceptors and the circadian clock initiate signals that regulate a network of genes in the leaf vascular system which communicates through mobile FLOWERING LOCUS T (FT) proteins, with the shoot apical meristem (SAM). At the SAM, a second network of genes is turned on specifically in certain cell domains, established by a second mobile protein, TERMINAL FLOWER 1 (TFL1), to ensure that flowering signals are translated into floral meristems at the flanks of the SAM but without compromising the nature of the SAM itself. Here, we provide an update on recent findings about the integration of light signals upstream of FT and tissue-specific events that occur in the SAM to balance flower production with SAM endurance.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Flores/genética , Flores/metabolismo , Regulação da Expressão Gênica de Plantas , Meristema/genética , Meristema/metabolismo , Fotoperíodo , Folhas de Planta/metabolismoRESUMO
Flowering is a rigorously timed and morphologically complex shift in plant development. This change depends on endogenous as well as environmental factors. FLOWERING LOCUS T (FT) integrates several cues from different pathways acting as a flowering promoter. Contrary to the role of FT, its paralog TERMINAL FLOWER 1 (TFL1) delays floral transition. Although FT/TFL1 homologs have been studied in model eudicots and monocots, scarce studies are available in non-model monocots like the Orchidaceae. Orchids are very diverse and their floral complexity is translated into a unique aesthetic display, which appeals the ornamental plant market. Nonetheless, orchid trade faces huge limitations due to their long vegetative phase and intractable indoor flowering seasons. Little is known about the genetic basis that control reproductive transition in orchids and, consequently, manipulating their flowering time remains a challenge. In order to contribute to the understanding of the genetic bases that control flowering in orchids we present here the first broad-scale analysis of FT/TFL1-like genes in monocots with an expanded sampling in Orchidaceae. We also compare expression patterns in three selected species and propose hypotheses on the putative role of these genes in their reproductive transition. Our findings show that FT-like genes are by far more diversified than TFL1-like genes in monocots with six subclades in the former and only one in the latter. Within MonFT1, the comparative protein sequences of MonFT1A and MonFT1B suggest that they could have recruited functional roles in delaying flowering, a role typically assigned to TFL1-like proteins. On the other hand, MonFT2 proteins have retained their canonical motifs and roles in promoting flowering transition. This is also shown by their increased expression levels from the shoot apical meristem (SAM) and leaves to inflorescence meristems (IM) and floral buds (FBs). Finally, TFL1-like genes are retained as single copy and often times are lost. Their loss could be linked to the parallel recruitment of MonFT1A and MonFT1B homologs in delaying flowering and maintaining indeterminacy of the inflorescence meristem. These hypotheses lay the foundation for future functional validation in emerging model orchid species and comparative analyses in orchids with high horticultural potential in the market.
RESUMO
A major issue in modern agriculture is water loss through stomata during photosynthetic carbon assimilation. In water-limited ecosystems, annual plants have strategies to synchronize their growth and reproduction to the availability of water. Some species or ecotypes of flowers are early to ensure that their life cycles are completed before the onset of late season terminal drought ("drought escape"). This accelerated flowering correlates with low water-use efficiency (WUE). The molecular players and physiological mechanisms involved in this coordination are not fully understood. We analyzed WUE using gravimetry, gas exchange, and carbon isotope discrimination in florigen deficient (sft mutant), wild-type (Micro-Tom), and florigen over-expressing (SFT-ox) tomato lines. Increased florigen expression led to accelerated flowering time and reduced WUE. The low WUE of SFT-ox was driven by higher stomatal conductance and thinner leaf blades. This florigen-driven effect on WUE appears be independent of abscisic acid (ABA). Our results open a new avenue to increase WUE in crops in an ABA-independent manner. Manipulation of florigen levels could allow us to produce crops with a life cycle synchronized to water availability.
Assuntos
Florígeno/metabolismo , Solanum lycopersicum/metabolismo , Água/fisiologia , Ácido Abscísico/metabolismo , Isótopos de Carbono/metabolismo , Produtos Agrícolas/genética , Produtos Agrícolas/metabolismo , Secas , Ecótipo , Flores/genética , Flores/metabolismo , Regulação da Expressão Gênica de Plantas , Solanum lycopersicum/genética , Fotossíntese , Desenvolvimento Vegetal , Folhas de Planta/genética , Folhas de Planta/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Estômatos de Plantas/genética , Estômatos de Plantas/metabolismoRESUMO
Long days (LD) promote flowering of Arabidopsis thaliana compared with short days (SD) by activating the photoperiodic pathway. Here we show that growth under very-SD (3â h) or darkness (on sucrose) also accelerates flowering on a biological scale, indicating that SD actively repress flowering compared with very-SD. CONSTANS (CO) repressed flowering under SD, and the early flowering of co under SD required FLOWERING LOCUS T (FT). FT was expressed at a basal level in the leaves under SD, but these levels were not enhanced in co. This indicates that the action of CO in A. thaliana is not the mirror image of the action of its homologue in rice. In the apex, CO enhanced the expression of TERMINAL FLOWER 1 (TFL1) around the time when FT expression is important to promote flowering. Under SD, the tfl1 mutation was epistatic to co and in turn ft was epistatic to tfl1. These observations are consistent with the long-standing but not demonstrated model where CO can inhibit FT induction of flowering by affecting TFL1 expression.