Light intensity modulates the regulatory network of the shade avoidance response in Arabidopsis.

Plants such as Arabidopsis thaliana respond to foliar shade and neighbors who may become competitors for light resources by elongation growth to secure access to unfiltered sunlight. Challenges faced during this shade avoidance response (SAR) are different under a light-absorbing canopy and during neighbor detection where light remains abundant. In both situations, elongation growth depends on auxin and transcription factors of the phytochrome interacting factor (PIF) class. Using a computational modeling approach to study the SAR regulatory network, we identify and experimentally validate a previously unidentified role for long hypocotyl in far red 1, a negative regulator of the PIFs. Moreover, we find that during neighbor detection, growth is promoted primarily by the production of auxin. In contrast, in true shade, the system operates with less auxin but with an increased sensitivity to the hormonal signal. Our data suggest that this latter signal is less robust, which may reflect a cost-to-robustness tradeoff, a system trait long recognized by engineers and forming the basis of information theory

Influence of diffraction on the spectrum and wavefunctions of an open system

In this paper, we demonstrate the existence and significance of diffractive orbits in an open microwave billiard, both experimentally and theoretically. Orbits that diffract off of a sharp edge of the system are found to have a strong influence on the transmission spectrum of the system, especially in the regime where there are no stable classical orbits. On resonance, the wavefunctions are influenced by both classical and diffractive orbits. Off resonance, the wavefunctions are determined by the constructive interference of multiple transient, nonperiodic orbits. Experimental, numerical, and semiclassical results are presented.Comment: 27 pages, 29 figures, and 3 tables. Submitted to Physical Review E. A copy with higher resolution figures is available at http://monsoon.harvard.edu/~hersch/papers.htm

High capacity in G protein-coupled receptor signaling.

G protein-coupled receptors (GPCRs) constitute a large family of receptors that activate intracellular signaling pathways upon detecting specific extracellular ligands. While many aspects of GPCR signaling have been uncovered through decades of studies, some fundamental properties, like its channel capacity-a measure of how much information a given transmission system can reliably transduce-are still debated. Previous studies concluded that GPCRs in individual cells could transmit around one bit of information about the concentration of the ligands, allowing only for a reliable on or off response. Using muscarinic receptor-induced calcium response measured in individual cells upon repeated stimulation, we show that GPCR signaling systems possess a significantly higher capacity. We estimate the channel capacity of this system to be above two, implying that at least four concentration levels of the agonist can be distinguished reliably. These findings shed light on the basic principles of GPCR signaling

Nuclear phytochrome a signaling promotes phototropism in Arabidopsis.

Phototropin photoreceptors (phot1 and phot2 in Arabidopsis thaliana) enable responses to directional light cues (e.g., positive phototropism in the hypocotyl). In Arabidopsis, phot1 is essential for phototropism in response to low light, a response that is also modulated by phytochrome A (phyA), representing a classical example of photoreceptor coaction. The molecular mechanisms underlying promotion of phototropism by phyA remain unclear. Most phyA responses require nuclear accumulation of the photoreceptor, but interestingly, it has been proposed that cytosolic phyA promotes phototropism. By comparing the kinetics of phototropism in seedlings with different subcellular localizations of phyA, we show that nuclear phyA accelerates the phototropic response, whereas in the fhy1 fhl mutant, in which phyA remains in the cytosol, phototropic bending is slower than in the wild type. Consistent with this data, we find that transcription factors needed for full phyA responses are needed for normal phototropism. Moreover, we show that phyA is the primary photoreceptor promoting the expression of phototropism regulators in low light (e.g., PHYTOCHROME KINASE SUBSTRATE1 [PKS1] and ROOT PHOTO TROPISM2 [RPT2]). Although phyA remains cytosolic in fhy1 fhl, induction of PKS1 and RPT2 expression still occurs in fhy1 fhl, indicating that a low level of nuclear phyA signaling is still present in fhy1 fhl

Color gamut reduction techniques for printing with custom inks

Printing with custom inks is of interest both for artistic purposes and for printing security documents such as banknotes. However, in order to create designs with only a few custom inks, a general purpose high-quality gamut reduction technique is needed. Most existing gamut mapping techniques map an input gamut such as the gamut of a CRT display into the gamut of an output device such as a CMYK printer. In the present contribution, we are interested in printing with up to three custom inks, which in the general case define a rather narrow color gamut compared with the gamut of standard CMYK printers. The proposed color gamut reduction techniques should work for any combination of custom inks and have a smooth and predictable behavior. When the black ink is available, the lightness levels present in the original image remain nearly identical. Original colors with hues outside the target gamut are projected onto the gray axis. Original colors with hues inside the target gamut hues are rendered as faithful as possible. When the black ink is not available, we map the gray axis G into a colored curve G' connecting in the 3D color space the paper white and the darkest available color formed by the superposition of the 3 inks. The mapped gray axis curve G' is given by the Neugebauer equations when enforcing equal amounts of custom inks. After lightness mapping, hue and saturation mappings are carried out. When the target gamut does not incorporate the gray axis, we divide it into two volumes, one on the desaturated side of the mapped gray axis curve G' and the other on the saturated side of the G' curve. Colors whose hues are not part of the target color gamut are mapped to colors located on the desaturated side of the G' curve. Colors within the set of printable hues remain within the target color gamut and retain as much as possible their original hue and saturatio

Maximizing Neumann fundamental tones of triangles

We prove sharp isoperimetric inequalities for Neumann eigenvalues of the Laplacian on triangular domains. The first nonzero Neumann eigenvalue is shown to be maximal for the equilateral triangle among all triangles of given perimeter, and hence among all triangles of given area. Similar results are proved for the harmonic and arithmetic means of the first two nonzero eigenvalues

Observation of diffractive orbits in the spectrum of excited NO in a magnetic field

We investigate the experimental spectra of excited NO molecules in the diamagnetic regime and develop a quantitative semiclassical framework to account for the results. We show the dynamics can be interpreted in terms of classical orbits provided that in addition to the geometric orbits, diffractive effects are appropriately taken into account. We also show how individual orbits can be extracted from the experimental signal and use this procedure to reveal the first experimental manifestation of inelastic diffractive orbits.Comment: 4 fig

Distinct levels in Pom1 gradients limit Cdr2 activity and localization to time and position division.

Where and when cells divide are fundamental questions. In rod-shaped fission yeast cells, the DYRK-family kinase Pom1 is organized in concentration gradients from cell poles and controls cell division timing and positioning. Pom1 gradients restrict to mid-cell the SAD-like kinase Cdr2, which recruits Mid1/Anillin for medial division. Pom1 also delays mitotic commitment through Cdr2, which inhibits Wee1. Here, we describe quantitatively the distributions of cortical Pom1 and Cdr2. These reveal low profile overlap contrasting with previous whole-cell measurements and Cdr2 levels increase with cell elongation, raising the possibility that Pom1 regulates mitotic commitment by controlling Cdr2 medial levels. However, we show that distinct thresholds of Pom1 activity define the timing and positioning of division. Three conditions-a separation-of-function Pom1 allele, partial downregulation of Pom1 activity, and haploinsufficiency in diploid cells-yield cells that divide early, similar to pom1 deletion, but medially, like wild-type cells. In these cells, Cdr2 is localized correctly at mid-cell. Further, Cdr2 overexpression promotes precocious mitosis only in absence of Pom1. Thus, Pom1 inhibits Cdr2 for mitotic commitment independently of regulating its localization or cortical levels. Indeed, we show Pom1 restricts Cdr2 activity through phosphorylation of a C-terminal self-inhibitory tail. In summary, our results demonstrate that distinct levels in Pom1 gradients delineate a medial Cdr2 domain, for cell division placement, and control its activity, for mitotic commitment