Genetic disorders of the Ras/MAPK pathway, termed RASopathies, produce numerous abnormalities, including cutaneous keratodermas. The desmosomal cadherin, desmoglein-1 (DSG1), promotes keratinocyte differentiation by attenuating MAPK/ERK signaling and is linked to striate palmoplantar keratoderma (SPPK). This raises the possibility that cutaneous defects associated with SPPK and RASopathies share certain molecular faults. To identify intermediates responsible for executing the inhibition of ERK by DSG1, we conducted a yeast 2-hybrid screen. The screen revealed that Erbin (also known as ERBB2IP), a known ERK regulator, binds DSG1. Erbin silencing disrupted keratinocyte differentiation in culture, mimicking aspects of DSG1 deficiency. Furthermore, ERK inhibition and the induction of differentiation markers by DSG1 required both Erbin and DSG1 domains that participate in binding Erbin. Erbin blocks ERK signaling by interacting with and disrupting Ras-Raf scaffolds mediated by SHOC2, a protein genetically linked to the RASopathy, Noonan-like syndrome with loose anagen hair (NS/LAH). DSG1 overexpression enhanced this inhibitory function, increasing Erbin-SHOC2 interactions and decreasing Ras-SHOC2 interactions. Conversely, analysis of epidermis from DSG1-deficient patients with SPPK demonstrated increased Ras-SHOC2 colocalization and decreased Erbin-SHOC2 colocalization, offering a possible explanation for the observed epidermal defects. These findings suggest a mechanism by which DSG1 and Erbin cooperate to repress MAPK signaling and promote keratinocyte differentiation.

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The goal of this research was to determine the potential for use of site-specific management of corn hybrids and plant densities in dryland landscapes of the Great Plains by determining (1) within-field yield variation, (2) yield response of different hybrids and plant densities to variability, and (3) landscape attributes associated with yield variation. This work was conducted on three adjacent fields in eastern Colorado during the 1997,-98, and-99 seasons. Treatments consisted of a combination of two hybrids (early and late maturity) and four plant densities (24,692, 37,037, 49,382 and 61,727 plants ha)1) seeded in replicated long strips. At maturity, yield was measured with a yield-mapping combine. Nine landscape attributes including elevation, slope, soil brightness (SB) (red, green, and blue bands of image), EC a (shallow and deep readings), pH, and soil organic matter (SOM) were also assessed. An analysis of treatment yields and landscape data, to assess for spatial dependency, along with semi variance analysis, and block kriging were used to produce kriged layers (10 m grids). Linear correlation and multiple linear regression analysis were used to determine associations between kriged average yields and landscape attributes. Yield monitor data revealed considerable variability in the three fields, with average yields ranging from 5.43 to 6.39 mg ha)1 and CVs ranging from 20% to 29%. Hybrids responded similarly to field variation while plant densities responded differentially. Economically optimum plant densities changed by around 5000 plants ha)1 between high and low-yielding field areas, producing a potential savings in seed costs of $6.25 ha)1. Variability in yield across the three landscapes was highly associated with landscape attributes, especially elevation and SB, with various combinations of landscape attributes accounting for 47%, 95%, and 76% of the spatial variability in grain yields for the 1997,-98, and-99 sites, respectively. Our results suggest site-specific management of plant densities may be feasible.

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Epidermal structure is damaged by exposure to ultraviolet (UV) light but the molecular mechanisms governing structural repair are largely unknown. UVB (290-320 nm wavelengths) exposure prior to induction of differentiation reduced expression of differentiation-associated proteins, including Desmoglein 1 (Dsg1), Desmocollin 1 (Dsc1) and Keratins 1 and 10 (K1/K10) in a dose-dependent manner in normal human epidermal keratinocytes (NHEKs). The UVB- induced reduction in both Dsg1 transcript and protein was associated with reduced binding of the p63 transcription factor to previously unreported enhancer regulatory regions of the Dsg1 gene. Since Dsg1 promotes epidermal differentiation in addition to participating in cell-cell adhesion, the role of Dsg1 in aiding differentiation after UVB damage was tested. Compared to controls, depleting Dsg1 via shRNA resulted in further reduction of Dsc1 and K1/K10 expression in monolayer NHEK cultures and in abnormal epidermal architecture in organotypic skin models recovering from UVB exposure. Ectopic expression of Dsg1 in keratinocyte monolayers rescued the UVB-induced differentiation defect. Treatment of UVB-exposed monolayer or organotypic cultures with Trichostatin A, a histone deacetylase inhibitor, partially restored differentiation marker expression, suggesting a potential therapeutic strategy for reversing UV-induced impairment of epidermal differentiation after acute sun exposure.

The epidermis is the first line of defense against ultraviolet (UV) light from the sun. Keratinocytes and melanocytes respond to UV exposure by eliciting a tanning response dependent in part on paracrine signaling, but how keratinocyte:melanocyte communication is regulated during this response remains understudied. Here, we uncover a surprising new function for the keratinocyte‐specific cell–cell adhesion molecule desmoglein 1 (Dsg1) in regulating keratinocyte:melanocyte paracrine signaling to promote the tanning response in the absence of UV exposure. Melanocytes within Dsg1‐silenced human skin equivalents exhibited increased pigmentation and altered dendrite morphology, phenotypes which were confirmed in 2D culture using conditioned media from Dsg1‐silenced keratinocytes. Dsg1‐silenced keratinocytes increased melanocyte‐stimulating hormone precursor (Pomc) and cytokine mRNA. Melanocytes cultured in media conditioned by Dsg1‐silenced keratinocytes increased Mitf and Tyrp1 mRNA, TYRP1 protein, and melanin production and secretion. Melanocytes in Dsg1‐silenced skin equivalents mislocalized suprabasally, reminiscent of early melanoma pagetoid behavior. Together with our previous report that UV reduces Dsg1 expression, these data support a role for Dsg1 in controlling keratinocyte:melanocyte paracrine communication and raise the possibility that a Dsg1‐deficient niche contributes to pagetoid behavior, such as occurs in early melanoma development.

Canola oil is high in oleic acid which is commonly used for food and industrial purposes. To determine adaptability of spring canola (Brassica napus L.) to the High Plains for industrial oil production, 26 irrigated trials were conducted from 2005 to 2008. Trials were divided into five regions-1: 36-37 • N 108 • W; 2: 39-40 • N 101-103 • W; 3: 41-42 • N 102-103 • W; 4: 41-42 • N 104 • W; 5: 43-44 • N 106-108 • W. Cultural practices were based on site-specific protocols. Four cultivars, Hyola 401, Hyola 357 Magnum, SW Marksman, and SW Patriot, were planted in replicated plots in April or May under standard irrigation and harvested in July to October depending on region. Seed yield Hyola 401 and Hyola 357 Magnum were higher than SW Marksman and SW Patriot across the five regions and within Regions 1, 2, 3, and 5. Regions 1, 2 and 3 yielded significantly greater than did Regions 4 and 5. Samples from 18 trials were examined for their oil content and fatty acid distribution. The four cultivars had greater than 38% oil content; SW Marksman and SW Patriot had higher oil content than Hyola 401 and Hyola 357 Mag. Higher oil content was achieved in Regions 1, 4 and 5. Across and within regions, the percent of oleic acid did not differ for the four cultivars. The mean content of oleic acid decreased going north from Region 2 to Region 5, as did seed yield in the High Plains. Linoleic acid increased going north from Region 1. Linolenic acids showed little variation across regions. Considering yield and total oil content together, growing spring canola would be excellent in the High Plains.