Plants constantly sense the changes in their environment; when mineral elements are scarce, they often allocate a greater proportion of their biomass to the root system. This acclimatory response is a consequence of metabolic changes in the shoot and an adjustment of carbohydrate transport to the root. It has long been known that deficiencies of essential macronutrients (nitrogen, phosphorus, potassium and magnesium) result in an accumulation of carbohydrates in leaves and roots, and modify the shoot-to-root biomass ratio. Here, we present an update on the effects of mineral deficiencies on the expression of genes involved in primary metabolism in the shoot, the evidence for increased carbohydrate concentrations and altered biomass allocation between shoot and root, and the consequences of these changes on the growth and morphology of the plant root system. Responses of plants to mineral deficienciesPlant growth and development ultimately depend upon environmental variables, such as temperature, light intensity and the availability of water and essential minerals. One of the mechanisms by which plants adjust to an imbalance of exogenous resources is by allocating new biomass to the organs that are involved in acquiring the resources that are scarcest [1]. Studies examining the relationships between mineral nutrition and plant growth and development have been undertaken, but most work has focussed on elucidating ion transport mechanisms and the biochemical pathways affected by mineral deficiencies [2][3][4]. Many reviews provide a comprehensive picture of the nature of mineral acquisition from the soil, transport within the plant and homeostasis in the plant cell [5][6][7][8][9][10]. However, progress is slow in understanding the molecular and physiological events responsible for sensing and signalling mineral resource limitation and their ultimate effects on plant development and biomass allocation. Now, with the emergence of microarray technologies to monitor gene expression, plant physiologists have begun to investigate the rapid transcriptional changes associated with mineral imbalance [11][12][13][14][15][16][17][18][19][20][21][22][23]. There is also considerable interest in the functional connection between the genome and the complement of ions in the cell (the ionome) [24].Deficiencies of nitrogen (N) [20,[25][26][27][28][29][30][31] and phosphorus (P) [7,[32][33][34][35][36][37] result in accumulation of carbohydrate in leaves, higher levels of carbon allocated to the root and an increase in root-to-shoot (R:S) biomass ratio. N and P deficiencies therefore affect, to various extents, primary photosynthesis, sugar metabolism and/or carbohydrate partitioning between source and sink tissues. By contrast, although leaves of potassium (K)-deficient [32,33,38,39] and magnesium (Mg)-deficient [32,33,[40][41][42][43] plants accumulate sugars, they rarely increase their root biomass. This is likely to be a consequence of impaired sucrose export from leaves of K-and Mg-deficient plants, rather than a change in p...

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The circadian clock is an endogenous timekeeper that allows organisms to anticipate and adapt to the daily variations of their environment. The plant clock is an intricate network of interlocked feedback loops, in which transcription factors regulate each other to generate oscillations with expression peaks at specific times of the day. Over the last decade, mathematical modeling approaches have been used to understand the inner workings of the clock in the model plant Arabidopsis thaliana. Those efforts have produced a number of models of ever increasing complexity. Here, we present an alternative model that combines a low number of equations and parameters, similar to the very earliest models, with the complex network structure found in more recent ones. This simple model describes the temporal evolution of the abundance of eight clock gene mRNA/protein and captures key features of the clock on a qualitative level, namely the entrained and free-running behaviors of the wild type clock, as well as the defects found in knockout mutants (such as altered free-running periods, lack of entrainment, or changes in the expression of other clock genes). Additionally, our model produces complex responses to various light cues, such as extreme photoperiods and non-24 h environmental cycles, and can describe the control of hypocotyl growth by the clock. Our model constitutes a useful tool to probe dynamical properties of the core clock as well as clock-dependent processes.