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Highlights An existing sugar beet crop coefficient curve (K cr ) was modified to better represent canopy development in northeast Colorado conditions. The modified K cr curve improved the estimated soil water deficits (net irrigation requirements) calculated by the cloud-based Water Irrigation Scheduler for Efficient Application (WISE App). Feedback from sugar beet growers and agronomists helped expand WISE applicability in the northern High Plains with access to additional weather station networks and functionality to aggregate irrigation data across multiple sugar beet fields or regions. Abstract . The convergence of agrometeorological network, database, and cloud-computing technologies has enabled greater accessibility of irrigation management tools for growers. The goal of this research and outreach project was to adapt an existing cloud-based irrigation scheduler (WISE) for use by sugar beet (Beta vulgaris L.) producers in eastern Colorado and a wider area of a cooperative operating in Colorado, Nebraska, Wyoming, and Montana. Four center pivot sugar beet fields in northeast Colorado were monitored during the 2013 and 2014 growing seasons. Soil water, leaf area index (LAI), and weather data were used to estimate the soil water deficit (net irrigation requirement) and to modify a crop coefficient (Kcr) curve originally reported in the literature based on growing degree days (GDD). The average cumulative GDDs for sugar beets to mature (100% maturity) was 2,944°C·d. The localized Kcr had a peak value (Kcr,mid) occurring between 43% and 69% of maturity, which corresponded to effective full cover (LAI = 3) and start of leaf senescence, respectively. In contrast, the original Kcr curve from literature had a longer duration of Kcr,mid spanning 33% to 83% of maturity. Use of the modified Kcr curve in lieu of the original Kcr curve in WISE reduced the relative error of soil water deficits by 12% to 35%. Feedback and collaborations from representative sugar beet growers and agronomists in the Western Sugar Cooperative led to expansion of WISE weather data access in the High Plains to include sugar beet growing areas in western Nebraska, eastern and northern Wyoming, and southern Montana. Keywords: Crop coefficient, Evapotranspiration, Irrigation scheduling, Soil water balance, Soil water deficit, Sugar beets.

The glucocorticoid receptor (GR) has been shown to be important for mediating cellular responses to stress and circulating glucocorticoids. Ligand-dependent transcriptional changes induced by GR are observed across numerous tissues. However, the mechanisms by which GR achieves cell and tissue-specific effects are less clear. Epigenetic mechanisms have been proposed to explain some of these differences as well as some of the lasting, even transgenerational, effects of stress and glucocorticoid action. GR functions in tandem with epigenetic cellular machinery to coordinate transcription and shape chromatin structure. Here, we describe GR interactions with these effectors and how GR acts to reshape the epigenetic landscape in response to the environment.

Adaptation to the environment is indispensable for organismal fitness. The brain is responsible for detection of and adaptation to stressful stimuli. Few molecular mechanisms facilitating this response have been described including neuronal plasticity, neurogenesis, and changes in gene expression. With the advent of next-generation sequencing technologies, large swathes of the noncoding genome have been identified and a role for the deep genome in governing the neural response to stress has been outlined. For instance, in the hippocampus heterochromatin remodeling is observed in gene deserts, here, marking repetitive retroelements selectively for transcriptional silencing. Aberrant retroelement expression is predicted to contribute to functional deficits in stress-sensitive brain regions. Though not yet fully realized, this “junk” represents a novel frontier in stress physiology relevant to many stress-related pathologies.

The brain is responsible for both recognition and adaptation to stressful stimuli. Many molecular mechanisms have been implicated in this response including those governing neuronal plasticity, neurogenesis and, changes gene expression. Far less is known regarding effects of stress on the deep genome. In the hippocampus, stress appears to regulate expression of non-coding elements of the genome as well as the chromatin permissive for their transcription. Specifically, hippocampal retrotransposon (RT) elements are regulated by acute stress via the accumulation of the repressive H3K9me3 mark at RT loci. Further, corticosteroids appear to induce changes in heterochromatin status as well as RT expression in both adrenalectomized animal and rat cell culture models. Dysregulation of RT expression is predicted to result in functional deficits in affected brain areas. More broadly, however, transposons may have a variety of adaptive functions. As techniques improve to probe the deep genome, this approach to understanding stress neurobiology has the potential to yield insights into environment and genome interactions that may contribute to the physiology underlying a number of stress-related mental health disorders.

The hippocampus is a highly plastic brain region sensitive to environmental stress. It shows dynamic changes in epigenetic marks associated with stress related learning. Previous work has shown that acute stress induces substantial transient changes in histone H3 lysine 9 trimethylation (H3K9me3). Moreover, increased H3K9me3 is enriched in hippocampal gene deserts accumulating within endogenous retroviruses and transposable elements. We have found that in response to acute glucocorticoid treatment, a similar change in global H3K9me3 is observed. However, when localized we found that H3K9me3 is markedly decreased at B2 short interspersed nuclear elements but not within intracisternal-A particle endogenous retroviruses. Further, decreased H3K9me3 valence within B2 elements was associated with increased transcript abundance. These data demonstrate the capacity for acute glucocorticoids to mobilize transposable elements via epigenetic unmasking. Reconciled with previous findings following acute stress, this suggests the capacity for mobile elements to potentially function as novel regulators given their dynamic regulation by stress and glucocorticoids.

Neuropsychiatric disorders are highly prevalent (e.g., affecting children 2-8 years old at a rate of 14%). Many of these disorders are highly heritable such as major depressive disorder and schizophrenia. Despite this, genome-wide association has failed to identify gene(s) significantly associated with diagnostic status suggesting a strong role for environmental factors and the epigenome. From a molecular standpoint, the study of DNA-protein interactions yields fruitful information regarding the regulation of cellular processes above the level of the nucleotide sequence. Understanding chromatin dynamics may continue to explain individual variation to environmental perturbation and subsequent behavioral response. Chromatin immunoprecipitation (ChIP) techniques have allowed for probing of epigenetic effectors at specific regions of the genome. The following article reviews the current techniques and considerations when incorporation ChIP into neuropsychiatric models.

Oxytocin is important for postnatal developmental experiences for mothers, infants, and transactions between them. Oxytocin is also implicated in adult affiliative behaviors, including social buffering of stress. There is evidence for connections between early life experience and adult oxytocin system functioning, but effects of early experience on behavioral, endocrine, and neurophysiological outcomes related to adult social buffering are not well explored. We use a limited bedding and nesting (LBN) material paradigm as an environmental disruption of early experiences and assessed central oxytocin systems in brain regions related to hypothalamic-pituitary-adrenal (HPA) axis regulation (paraventricular nucleus of the hypothalamus, amygdala, hippocampus). We also assessed developmentally-appropriate social behaviors and HPA reactivity during social buffering testing in adulthood. LBN litters had larger huddles and more pups visible compared to control litters during the first two weeks of life. LBN also altered the developmental trajectory of oxytocin-expressing cells and oxytocin receptor cells, with increases in oxytocin receptor cells at P15 in LBN pups. By adulthood, LBN females had more and LBN males had fewer oxytocin and oxytocin receptor cells in these areas compared to sex-matched controls. Adult LBN females, but not LBN males, had behavioral changes during social interaction and social buffering testing. The sex-specific effects of early experience on central oxytocin systems and social behavior may contribute to female resilience to early life adversity.

Expression of transposable elements (TE) is transiently activated during human preimplantation embryogenesis in a developmental stage- and cell type-specific manner and TE-mediated epigenetic regulation is intrinsically wired in developmental genetic networks in human embryos and embryonic stem cells. However, there are no systematic studies devoted to a comprehensive analysis of the TE transcriptome in human adult organs and tissues, including human neural tissues. To investigate TE expression in the human Dorsolateral Prefrontal Cortex (DLPFC), we developed and validated a straightforward analytical approach to chart quantitative genome-wide expression profiles of all annotated TE loci based on unambiguous mapping of discrete TE-encoded transcripts using a de novo assembly strategy. To initially evaluate the potential regulatory impact of DLPFC-expressed TE, we adopted a comparative evolutionary genomics approach across humans, primates, and rodents to document conservation patterns, lineage-specificity, and colocalizations with transcription factor binding sites mapped within primate- and human-specific TE. We identified 654,665 transcripts expressed from 477,507 distinct loci of different TE classes and families, the majority of which appear to have originated from primate-specific sequences. We discovered 4,687 human-specific and transcriptionally active TEs in DLPFC, of which the prominent majority (80.2%) appears spliced. Our analyses revealed significant associations of DLPFC-expressed TE with primate- and human-specific transcription factor binding sites, suggesting potential cross-talks of concordant regulatory functions. We identified 1,689 TEs differentially expressed in the DLPFC of Schizophrenia patients, a majority of which is located within introns of 1,137 protein-coding genes. Our findings imply that identified DLPFC-expressed TEs may affect human brain structures and functions following different evolutionary trajectories. On one side, hundreds of thousands of TEs maintained a remarkably high conservation for ∼8 My of primates’ evolution, suggesting that they are likely conveying evolutionary-constrained primate-specific regulatory functions. In parallel, thousands of transcriptionally active human-specific TE loci emerged more recently, suggesting that they could be relevant for human-specific behavioral or cognitive functions.

OBJECTIVES:: HIV-1 tropism needs to be determined before the use of CCR5 antagonist drugs such as maraviroc (MVC), which are ineffective against CXCR4-using HIV-1. This study assessed how different computational methods for predicting tropism from HIV sequence data performed in a large clinical cohort. The value of adding clinical data to these algorithms was also investigated. DESIGN AND METHODS:: PCR amplification and sequence analysis of the HIV-1 gp120 V3 loop region was performed on triple replicates of plasma viral RNA or proviral DNA extracted from peripheral blood monocytes (PBMCs) in 242 patients. Coreceptor usage was predicted from V3 sequences using seven bioinformatics interpretation algorithms, combined with clinical data where appropriate. An intention-to-treat approach was employed for exploring outcomes and performance for different viral subtypes was examined. RESULTS:: The frequency of R5 predictions varied by 22.6%, with all seven algorithms agreeing for only 75.3% of tests. The identification of individuals likely to fail was poor for all algorithms. The addition of clinical data improved this, but at the expense of their ability to predict success. The clinical algorithms varied across subtypes, whereas other algorithms were more consistent. Furthermore, individuals with discordant clonal and clinical predictions were more likely to fail MVC treatment. CONCLUSION:: Eligibility for MVC varied depending on the algorithm method used. The addition of clinical parameters alongside sequence data may help predict X4 emergence during treatment. It could be that V3 loop analysis in isolation may not be the best method for selecting individuals for MVC.