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Imperata cylindrica is a noxious weed that infests annual and perennial crops in most tropical regions. High crop densities may offer opportunities to reduce I. cylindrica competition in small-scale farming systems. The competitive ability of maize relative to I. cylindrica was evaluated in an addition series experiment in the forest savannah transition zone in 2006 and 2007 at Ibadan, Nigeria. Maize and I. cylindrica were planted in eight monoculture densities (4, 8, 12, 16, 20, 32, 48 and 64 plants m−2) and in a 1:1 mixture at eight total densities (2:2, 4:4, 6:6, 8:8, 10:10, 16:16, 24:24 and 32:32 maize: I. cylindrica plants m−2) as in monoculture. Non-linear regression models were used to relate crop and weed shoot biomass to their densities and total grain yield to maize density. In maize, intraspecific competition was more than interspecific competition; in I. cylindrica, interspecific competition was higher than intraspecific. As expected, total grain yield was lower in the mixture than in maize monoculture at all total densities. Average maize grain yield in maize monoculture differed from that in mixtures by 0.77 t ha−1 in 2006 and 0.57 t ha−1 in 2007. Niche differentiation indices were <1 in 2006 and >1 in 2007, indicating that both species competed for similar resources in 2006, but not in 2007. The greater competitive ability of maize over I. cylindrica may be associated with rapid growth and canopy development observed in the field. [ABSTRACT FROM AUTHOR]

Udensi K Udensi1,2, Barbara E Graham-Evans1, Christian Rogers1, Raphael D Isokpehi1,21RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217; 2Center for Bioinformatics & Computational Biology, Department of Biology, Jackson State University, PO Box 18540, Jackson MS 39217, USABackground: Arsenic is a ubiquitous environmental toxicant, and abnormalities of the skin are the most common outcomes of long-term, low-dose, chronic arsenic exposure. If the balance between keratinocyte proliferation, differentiation, and death is perturbed, pathologic changes of the epidermis may result, including psoriasis, atopic dermatitis, and certain forms of ichthyosis. Therefore, research investigations using in vitro human epidermal cells could help elucidate cellular and molecular processes in keratinocytes affected by arsenic. Data from such investigations could also provide the basis for developing cosmetic intervention for skin diseases caused by arsenic.Methods: The viability of HaCaT keratinocyte cultures with or without prior exposure to low-dose arsenic trioxide was compared for varying concentrations of arsenic trioxide over a time course of 14 days because in untreated control cultures, approximately 2 weeks is required to complete cell differentiation. Long-term cultures were established by culturing HaCaT cells on collagen IV, and cells were subsequently exposed to 0 parts per million (ppm), 1 ppm, 5 ppm, 7.5 ppm, 10 ppm, and 15 ppm of arsenic trioxide. The percentages of viable cells as well as DNA damage after exposure were determined on Day 2, Day 5, Day 8, and Day 14.Results: Using both statistical and visual analytics approaches for data analysis, we have observed a biphasic response at a 5 ppm dose with cell viability peaking on Day 8 in both chronic and acute exposures. Further, a low dose of 1 ppm arsenic trioxide enhanced HaCaT keratinocyte proliferation, whereas doses above 7.5 ppm inhibited growth.Conclusion: The time course profiling of arsenic trioxide cytotoxicity using long-term HaCaT keratinocyte cultures presents an approach to modeling the human epidermal cellular responses to varying doses of arsenic trioxide treatment or exposure. A low dose of arsenic trioxide appears to aid cell growth but concomitantly disrupts the DNA transcription process.Keywords: arsenic trioxide, chronic exposure, DNA damage, HaCaT, keratinocyte, visual analytics

Purpose: Corneal dysmorphologies (CDs) are typically classified as either regressive degenerative corneal dystrophies (CDtrs) or defective growth and differentiation-driven corneal dysplasias (CDyps). Both eye disorders have multifactorial etiologies. While previous work has elucidated many aspects of CDs, such as presenting symptoms, epidemiology, and pathophysiology, the genetic mechanisms remain incompletely understood. The purpose of this study was to analyze phenotype data from 8,707 knockout mouse lines to identify new genes associated with the development of CDs in humans., Methods: 8,707 knockout mouse lines phenotyped by the International Mouse Phenotyping Consortium were queried for genes associated with statistically significant (P < 0.0001) abnormal cornea morphology to identify candidate CD genes. Corneal abnormalities were investigated by histopathology. A literature search was used to determine the proportion of candidate genes previously associated with CDs in mice and humans. Phenotypes of human orthologues of mouse candidate genes were compared with known human CD genes to identify protein-protein interactions and molecular pathways using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), Protein Analysis Through Evolutionary Relationships (PANTHER), and Kyoto Encyclopedia of Genes and Genomes., Results: Analysis of data from 8,707 knockout mouse lines identified 213 candidate CD genes. Of these, 37 (17%) genes were previously known to be associated with CD, including 14 in the mouse, 16 in humans, and 7 in both. The remaining 176 (83%) genes have not been previously implicated in CD. We also searched publicly available RNAseq data and found that 131 of the total 213 (61.5%) were expressed in adult human corneal tissue. STRING analysis showed several interactions within and between candidate and established CD proteins. All cellular pathways of the established genes were found in the PANTHER analysis of the candidate genes. Several of the candidate genes were implicated in corneal disease, such as TGF-ß signaling. We also identified other possible underappreciated mechanisms relevant to the human cornea., Conclusions: We identified 213 mouse genes that resulted in statistically significant abnormal corneal phenotypes in knockout mice, many of which have not previously been implicated in corneal pathology. Bioinformatic analyses implicated candidate genes in several signaling pathways which are potential therapeutic targets., Competing Interests: Declarations. Ethics approval and consent to participate: All procedures at each IMPC center adhered to local, state, and national regulatory guidelines, based on the standards of Animal Research: Reporting of In Vivo Experiments guidelines, a list of recommendations to standardize and improve the quality and reproducibility of animal research. A Housing and Husbandry protocol was also followed, which contains a collection of mandatory and optional procedures to be used during international mouse experimentation.4,5 Guidelines can be accessed at https://www.mousephenotype.org/about-impc/animal-welfare/ . All procedures on live animals were reviewed and approved by associated institutional animal care and use committees (IACUC), animal care committees (ACC), or equivalent. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

[This corrects the article DOI: 10.1038/s42003-018-0226-0.].

Despite advances in next generation sequencing technologies, determining the genetic basis of ocular disease remains a major challenge due to the limited access and prohibitive cost of human forward genetics. Thus, less than 4,000 genes currently have available phenotype information for any organ system. Here we report the ophthalmic findings from the International Mouse Phenotyping Consortium, a large-scale functional genetic screen with the goal of generating and phenotyping a null mutant for every mouse gene. Of 4364 genes evaluated, 347 were identified to influence ocular phenotypes, 75% of which are entirely novel in ocular pathology. This discovery greatly increases the current number of genes known to contribute to ophthalmic disease, and it is likely that many of the genes will subsequently prove to be important in human ocular development and disease., Competing Interests: The authors declare no competing interests.

Retinal function relies on precisely organized neurons and synapses and a properly patterned vasculature to support them. Alterations in these features can result in vision loss. However, our understanding of retinal organization pathways remains incomplete because of a lack of methods to rapidly identify neuron and vasculature regulators in mammals. Here we developed a pipeline for the identification of neural and synaptic integrity genes by high-throughput retinal screening (INSiGHT) that analyzes candidate expression, vascular patterning, cellular organization, and synaptic arrangement. Using this system, we examined 102 mutant mouse lines and identified 16 unique retinal regulatory genes. Fifteen of these candidates are identified as novel retina regulators, and many (9 of 16) are associated with human neural diseases. These results expand the genetic landscape involved in retinal circuit organization and provide a road map for continued discovery of mammalian retinal regulators and disease-causing alleles., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)