Arabidopsis genome expression pattern changes in response to phosphate (Pi) starvation were examined during a 3-d period after removal of Pi from the growth medium. Available Pi concentration was decreased after the first 24 h of Pi starvation in roots by about 22%, followed by a slow recovery during the 2nd and 3rd d after Pi starvation, but no significant change was observed in leaves within the 3 d of Pi starvation. Microarray analysis revealed that more than 1,800 of the 6,172 genes present in the array were regulated by 2-fold or more within 72 h from the onset of Pi starvation. Analysis of these Pi starvation-responsive genes shows that they belong to wide range of functional categories. Many genes for photosynthesis and nitrogen assimilation were down-regulated. A complex set of metabolic adaptations appears to occur during Pi starvation. More than 100 genes each for transcription factors and cell-signaling proteins were regulated in response to Pi starvation, implying major regulatory changes in cellular growth and development. A significant fraction of those regulatory genes exhibited distinct or even contrasting expression in leaves and roots in response to Pi starvation, supporting the idea that distinct Pi starvation response strategies are used for different plant organs in response to a shortage of Pi in the growth medium.Phosphorus is one of the three essential macronutrients of plants. Phosphorus is not only a constituent of such key cell molecules as ATP, nucleic acids, and phospholipids, but it is also a pivotal regulator in many metabolisms, including energy transfer, protein activation, and carbon and amino acid metabolic processes (Marschner, 1995). Limitation of phosphate (Pi) causes both molecular and developmental adaptation in all organisms. In higher plants, Pi limitation leads to dramatic changes in root growth and architecture, such as an increase root to shoot ratio, an increase of lateral roots, and an increase of root hair number and length, thus Pi use can be enhanced (Bates and Lynch, 1996;Rubio et al., 2001).Many molecular adaptation responses have been described from various organisms. For example, under Pi limitation, both Escherichia coli and Brewer's yeast (Saccharomyces cerevisiae) activate a multigeneinducible system to scavenge traces of usable Pi from the surrounding medium (Torriani, 1990;Lenburg and O'Shea, 1996). The existence of an analogous multigene Pi starvation-inducible system has also been proposed in higher plants based on studies with tomato (Lycopersicon esculentum) plants ( Goldstein et al., 1989). Several individual genes responsive to Pi starvation have been described. These include acid phosphatases with broad substrate specificity (Duff et al., 1994;Trull and Deikman, 1998), phosphoenolpyruvate (PEP) phosphatase and pyrophosphatedependent phosphofructokinase (Theodorou and Plaxto, 1993), RNases (Green, 1994), high-affinity Pi transporter (Raghothama, 2000), phosphodiesterases (Abel et al., 2000), ␤-glucosidase (Malboobi et al., 1998), and others of unkn...

Background Notch signaling in vascular smooth muscle precursors is required for smooth muscle differentiation. Jagged1 expression on endothelium activates Notch in vascular smooth muscle precursors including those of neural crest origin to initiate the formation of a smooth muscle layer in a maturing blood vessel. Methods and Results Here, we show that Jagged1 is a direct Notch target in smooth muscle, resulting in a positive feedback loop and lateral induction that propagates a wave of smooth muscle differentiation during aortic arch artery development. In vivo, we show that Notch inhibition in cardiac neural crest impairs Jagged1 mRNA expression and results in deficient smooth muscle differentiation and resultant aortic arch artery defects. Ex vivo, Jagged1 ligand activates Notch in neural crest explants and results in activation of Jagged1 mRNA, a response that is blocked by Notch inhibition. We examine 15 evolutionary conserved regions within the Jagged1 genomic locus and identify a single Notch response element within the second intron. This element contains a functional Rbp-J binding site demonstrated by luciferase reporter and chromatin immunoprecipitation assays and is sufficient to recapitulate aortic arch artery expression of Jagged1 in transgenic mice. Loss of Jagged1 in neural crest impairs vascular smooth muscle differentiation and results in aortic arch artery defects. Conclusions Taken together, these results provide a mechanism for lateral induction that allows for a multilayered smooth muscle wall to form around a nascent arterial endothelial tube and identify Jagged1 as a direct Notch target.

Cardiac progenitor cells are multipotent and give rise to cardiac endothelium, smooth muscle, and cardiomyocytes. Here, we define and characterize the cardiomyoblast intermediate that is committed to the cardiomyocyte fate, and we characterize the niche signals that regulate commitment. Cardiomyoblasts express Hopx, which functions to coordinate local Bmp signals to inhibit the Wnt pathway, thus promoting cardiomyogenesis. Hopx integrates Bmp and Wnt signaling by physically interacting with activated Smads and repressing Wnt genes. The identification of the committed cardiomyoblast that retains proliferative potential will inform cardiac regenerative therapeutics. In addition, Bmp signals characterize adult stem cell niches in other tissues where Hopx-mediated inhibition of Wnt is likely to contribute to stem cell quiescence and to explain the role of Hopx as a tumor suppressor.