Mathematical Modeling of Photo- and Thermomorphogenesis in Plants.

Increased day lengths and warm conditions inversely affect plant growth by directly modulating nuclear phyB, ELF3, and COP1 levels. Quantitative measures of the hypocotyl length have been key to gaining a deeper understanding of this complex regulatory network, while similar quantitative data are the foundation for many studies in plant biology. Here, we explore the application of mathematical modeling, specifically ordinary differential equations (ODEs), to understand plant responses to these environmental cues. We provide a comprehensive guide to constructing, simulating, and fitting these models to data, using the law of mass action to study the evolution of molecular species. The fundamental principles of these models are introduced, highlighting their utility in deciphering complex plant physiological interactions and testing hypotheses. This brief introduction will not allow experimentalists without a mathematical background to run their own simulations overnight, but it will help them grasp modeling principles and communicate with more theory-inclined colleagues.

Two modes of gene regulation by TFL1 mediate its dual function in flowering time and shoot determinacy of Arabidopsis.

Plant organ primordia develop successively at the shoot apical meristem (SAM). In Arabidopsis, primordia formed early in development differentiate into vegetative leaves, whereas those formed later generate inflorescence branches and flowers. TERMINAL FLOWER 1 (TFL1), a negative regulator of transcription, acts in the SAM to delay flowering and to maintain inflorescence meristem indeterminacy. We used confocal microscopy, time-resolved transcript profiling and reverse genetics to elucidate this dual role of TFL1. We found that TFL1 accumulates dynamically in the SAM reflecting its dual function. Moreover, TFL1 represses two major sets of genes. One set includes genes that promote flowering, expression of which increases earlier in tfl1 mutants. The other set is spatially misexpressed in tfl1 inflorescence meristems. The misexpression of these two gene sets in tfl1 mutants depends upon FD transcription factor, with which TFL1 interacts. Furthermore, the MADS-box gene SEPALLATA 4, which is upregulated in tfl1, contributes both to the floral transition and shoot determinacy defects of tfl1 mutants. Thus, we delineate the dual function of TFL1 in shoot development in terms of its dynamic spatial distribution and different modes of gene repression.