Using Light to Improve Commercial Value

The plasticity of plant morphology has evolved to maximize reproductive fitness in response to prevailing environmental conditions. Leaf architecture elaborates to maximize light harvesting, while the transition to flowering can either be accelerated or delayed to improve an individual's fitness. One of the most important environmental signals is light, with plants using light for both photosynthesis and as an environmental signal. Plants perceive different wavelengths of light using distinct photoreceptors. Recent advances in LED technology now enable light quality to be manipulated at a commercial scale, and as such opportunities now exist to take advantage of plants' developmental plasticity to enhance crop yield and quality through precise manipulation of a crops' lighting regime. This review will discuss how plants perceive and respond to light, and consider how these specific signaling pathways can be manipulated to improve crop yield and quality

Expression profiling during arabidopsis/downy mildew interaction reveals a highly-expressed effector that attenuates responses to salicylic acid

Plants have evolved strong innate immunity mechanisms, but successful pathogens evade or suppress plant immunity via effectors delivered into the plant cell. Hyaloperonospora arabidopsidis (Hpa) causes downy mildew on Arabidopsis thaliana, and a genome sequence is available for isolate Emoy2. Here, we exploit the availability of genome sequences for Hpa and Arabidopsis to measure gene-expression changes in both Hpa and Arabidopsis simultaneously during infection. Using a high-throughput cDNA tag sequencing method, we reveal expression patterns of Hpa predicted effectors and Arabidopsis genes in compatible and incompatible interactions, and promoter elements associated with Hpa genes expressed during infection. By resequencing Hpa isolate Waco9, we found it evades Arabidopsis resistance gene RPP1 through deletion of the cognate recognized effector ATR1. Arabidopsis salicylic acid (SA)-responsive genes including PR1 were activated not only at early time points in the incompatible interaction but also at late time points in the compatible interaction. By histochemical analysis, we found that Hpa suppresses SA-inducible PR1 expression, specifically in the haustoriated cells into which host-translocated effectors are delivered, but not in non-haustoriated adjacent cells. Finally, we found a highly-expressed Hpa effector candidate that suppresses responsiveness to SA. As this approach can be easily applied to host-pathogen interactions for which both host and pathogen genome sequences are available, this work opens the door towards transcriptome studies in infection biology that should help unravel pathogen infection strategies and the mechanisms by which host defense responses are overcome

Genome-wide activity of unliganded estrogen receptor-\u3b1\ua0 in breast cancer cells

Estrogen receptor-\u3b1 (ER\u3b1) has central role in hormone-dependent breast cancer and its ligand-induced functions have been extensively characterized. However, evidence exists that ER\u3b1 has functions that are independent of ligands. In the present work, we investigated the binding of ER\u3b1 to chromatin in the absence of ligands and its functions on gene regulation. We demonstrated that in MCF7 breast cancer cells unliganded ER\u3b1 binds to more than 4,000 chromatin sites. Unexpectedly, although almost entirely comprised in the larger group of estrogen-induced binding sites, we found that unliganded-ER\u3b1 binding is specifically linked to genes with developmental functions, compared with estrogen-induced binding. Moreover, we found that siRNA-mediated down-regulation of ER\u3b1 in absence of estrogen is accompanied by changes in the expression levels of hundreds of coding and noncoding RNAs. Down-regulatedmRNAs showed enrichment in genes related to epithelial cell growth and development. Stable ER\u3b1 down-regulation using shRNA, which caused cell growth arrest, was accompanied by increased H3K27me3 at ER\u3b1 binding sites. Finally, we found that FOXA1 and AP2\u3b3 binding to several sites is decreased upon ER\u3b1 silencing, suggesting that unliganded ER\u3b1 participates, together with other factors, in the maintenance of the luminal-specific cistrome in breast cancer cell

Effects of solar ultraviolet radiation on terrestrial ecosystems. Patterns, mechanisms, and interactions with climate change

Ultraviolet radiation (UV) is a minor fraction of the solar spectrum reaching the ground surface. In thisassessment we summarize the results of previous work on the effects of the UV-B component(280–315 nm) on terrestrial ecosystems, and draw attention to important knowledge gaps in ourunderstanding of the interactive effects of UV radiation and climate change. We highlight the followingpoints: (i) The effects of UV-B on the growth of terrestrial plants are relatively small and, because theMontreal Protocol has been successful in limiting ozone depletion, the reduction in plant growthcaused by increased UV-B radiation in areas affected by ozone decline since 1980 is unlikely to haveexceeded 6%. (ii) Solar UV-B radiation has large direct and indirect (plant-mediated) effects on canopyarthropods and microorganisms. Therefore, trophic interactions (herbivory, decomposition) interrestrial ecosystems appear to be sensitive to variations in UV-B irradiance. (iii) Future variations inUV radiation resulting from changes in climate and land-use may have more important consequenceson terrestrial ecosystems than the changes in UV caused by ozone depletion. This is because theresulting changes in UV radiation may affect a greater range of ecosystems, and will not be restrictedsolely to the UV-B component. (iv) Several ecosystem processes that are not particularly sensitive toUV-B radiation can be strongly affected by UV-A (315–400 nm) radiation. One example is the physicaldegradation of plant litter. Increased photodegradation (in response to reduced cloudiness or canopycover) will lead to increased carbon release to the atmosphere via direct and indirect mechanisms