Effects of Water Availability on Leaf Trichome Density and Plant Growth and Development of Shepherdia ×utahensis.

Many arid lands across the globe are experiencing more frequent and extreme droughts due to warmer temperatures resulting from climate change, less predictable precipitation patterns, and decreased soil moisture. Approximately 60-90% of household water is used for urban landscape irrigation in the western United States, necessitating the establishment of landscapes using drought-tolerant plants that conserve water. Shepherdia ×utahensis (hybrid buffaloberry) is a drought-tolerant plant with dense leaf trichomes (epidermal appendages) that may limit excessive water loss by transpiration. However, little is known about how S. ×utahensis regulates leaf heat balance when transpirational cooling is limited. The objective of this research was to investigate the effects of substrate water availability on plant growth and development and trichome density of S. ×utahensis. Ninety-six clonally propagated plants were grown using an automated irrigation system, and their substrate volumetric water contents were controlled at 0.05-0.40 m3·m-3 for 2 months. Results showed that water stress impaired plant growth and increased the proportion of visibly wilted leaves. Shepherdia ×utahensis acclimates to drought by reducing cell dehydration and canopy overheating, which may be accomplished through decreased stomatal conductance, smaller leaf development, leaf curling, increased leaf thickness, and greater root-to-shoot ratio. Leaf trichome density increased when stem water potential decreased, resulting in greater leaf reflectance of visible light. Cell and leaf expansion were restricted under water stress, and negative correlations were exhibited between epidermal cell size and trichome density. According to our results, plasticity in leaves and roots aids plants in tolerating abiotic stresses associated with drought. Acclimation of S. ×utahensis to water stress was associated with increased trichome density due to plasticity in cell size. Dense trichomes on leaves reflected more lights which appeared to facilitate leaf temperature regulation.

Nitrogen fertilizer form and associated nitrate leaching from cool-season lawn turf.

Various N fertilizer sources are available for lawn turf. Few field studies, however, have determined the losses of nitrate (NO(3)-N) from lawns receiving different formulations of N fertilizers. The objectives of this study were to determine the differences in NO(3)-N leaching losses among various N fertilizer sources and to ascertain when losses were most likely to occur. The field experiment was set out in a completely random design on a turf typical of the lawns in southern New England. Treatments consisted of four fertilizer sources with fast- and slow-release N formulations: (i) ammonium nitrate (AN), (ii) polymer-coated sulfur-coated urea (PCSCU), (iii) organic product, and (iv) a nonfertilized control. The experiment was conducted across three years and fertilized to supply a total of 147 kg N ha(-1) yr(-1). Percolate was collected with zero-tension lysimeters. Flow-weighted NO(3)-N concentrations were 4.6, 0.57, 0.31, and 0.18 mg L(-1) for AN, PCSCU, organic, and the control, respectively. After correcting for control losses, average annual NO(3)-N leaching losses as a percentage of N applied were 16.8% for AN, 1.7% for PCSCU, and 0.6% for organic. Results indicate that NO(3)-N leaching losses from lawn turf in southern New England occur primarily during the late fall through the early spring. To reduce the threat of NO(3)-N leaching losses, lawn turf fertilizers should be formulated with a larger percentage of slow-release N than soluble N.

Comparison of the clinical expression of retinitis pigmentosa associated with rhodopsin mutations at codon 347 and codon 23.

PURPOSE: To examine the difference in expression of retinitis pigmentosa from mutations at codon 23 and codon 347 or rhodopsin; to report a novel mutation in rhodopsin. METHODS: Goldmann perimetry (solid angle of I4e isopter) and electroretinographic amplitudes (square root transform of a response ratio) were analyzed for 24 patients with mutations at codon 347 (15 with Pro347Ala, 2 with Pro347Gln, 6 with Pro347Leu, and 1 with a novel Pro347Cys change) and 41 patients with mutations at codon 23 (6 with Pro23Ala; 35 with Pro23His). RESULTS: When all patients with mutations at codons 347 and 23 were compared, loss of visual fields was significantly worse in patients with codon 347 changes (P =.0003). Only rod responses of the electroretinograms were significantly different between the two groups (P =.048). Specific comparison of Pro347Ala with Pro23Ala using regression analysis demonstrated significant differences in severity between codon 23 and codon 347 patients for b-wave amplitudes of rod (P =.0069), cone (P =.039) and maximum combined response (P =.049). The solid angle of the I4e isopter was also significantly different (P =.025) between the groups after controlling for age. Modeling age by group for Pro347Ala comparison produced an R(2) of.44. CONCLUSION: We reconfirmed that rhodopsin-related retinitis pigmentosa from mutations involving codon 347 produces a more severe phenotype than that involving codon 23. Accurate modeling of disease was shown to be possible by incorporating the effects of a patient's age and specific genotype. Therefore, both of these variables must be considered in prognostic counseling and subject recruitment for future therapeutic trials.

VSX1: a gene for posterior polymorphous dystrophy and keratoconus.

We identified mutations in the VSX1 homeobox gene for two distinct inherited corneal dystrophies; posterior polymorphous dystrophy (PPD) and keratoconus. One of the mutation (R166W) responsible for keratoconus altered the homeodomain and impaired DNA binding. Two other sequence changes (L159M and G160D) were associated with keratoconus and PPD, respectively, and involved a region adjacent to the homeodomain. The G160D substitution, and a fourth defect affecting the highly conserved CVC domain (P247R), occurred in a child with very severe PPD who required a corneal transplant at 3 months of age. In this family, relatives with the G160D change alone had mild to moderate PPD, while P247R alone caused no corneal abnormalities. However, with either the G160D or P247R mutation, electroretinography detected abnormal function of the inner retina, where VSX1 is expressed. These data define the molecular basis of two important corneal dystrophies and reveal the importance of the CVC domain in the human retina.