Provided herein are methods of inducing psychosis in animals using light-responsive opsins and methods of identifying or screening compounds that may be useful in treating psychosis.

The invention provides a method of modulating electrophysiological activity of an excitable cell. The method involves causing exogenous expression of a glycine receptor (GlyR) protein in an excitable cell of a subject. Thereafter, the excitable cell is exposed to an allosteric modulator of the GlyR protein. Modulation of the exogenous GlyR protein (an ion channel) in response to the allosteric modulator modulates the electrophysiological activity of the excitable cell. The method can be used to control pain in a subject. The invention further provides a replication-defective HSV vector comprising an expression cassette encoding a GlyR protein, stocks and pharmaceutical compositions containing such vectors, and a transgenic animal.

The present invention relates to the field of fibrosis and inflammation and more particularly to the use of ADAM12 (A Disintegrin and Metalloproteinase 12) inhibitors to prevent or treat inflammation-induced fibrosis. The present invention also relates to the use of ADAM12 as a marker for inflammation-induced fibrosis and to the ablation of ADAM12 expressing cells as therapeutic approach to interfere with the development of pro-fibrotic cells.

The present invention to a method for expressing an exogenous gene specifically in cells of the retinal pigment epithelium N of a primate, this method comprising the step of delivering an isolated nucleic acid molecule comprising, or consisting of, the nucleic acid sequence of SEQ ID NO:1, or consisting of a nucleic acid sequence of at least 400 bp having at least 80% overall identity to the sequence of SEQ ID NO:1, to cells of the retinal pigment epithelium of the primate, wherein this isolated nucleic acid molecule specifically leads to the expression of an exogenous gene in cells of the retinal pigment epithelium of primates when a nucleic acid sequence coding for the exogenous gene is operatively linked to this isolated nucleic acid molecule.

The present disclosure is directed, in some embodiments, to compositions and methods for inducible modification of a cell genome.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) CD47, and methods of use thereof.

Methods for elucidating biopolymer interactions with known and/or unknown small molecules (e.g. candidate drug compounds) are disclosed. These methods utilize novel (usually motile) organisms transformed with one or more heterologous biopolymer sequences. Biopolymer expression is promoted in cells mediating movement in said organism, generally dually-promoted in paired sets of cells mediating oppositely-directed movement. Modulation of motility in the resultant organism due to the presence of small molecules demonstrates small molecule interaction with said natural and/or mutated biopolymer. Analyzed in a chemical gradient, one or more interacting small molecule species can be identified by oriented migration, even in the presence of one or more non-interacting small molecule species. A competing and/or interfering biopolymer can be introduced without obscuring the motility signal. Methods described herein have utility for the discovery of novel therapeutic compounds (drug discovery), for the improvement of existing therapeutic compounds (drug refinement), and for the precise identification of small molecule binding sites on biopolymers via mutagenesis (structural elucidation). A specific embodiment, a Nematode Olfaction-based Structural Elucidation (NOSE) assay, is described herein.

A system is provided comprising a plurality of C. elegans cultures, where each culture comprises a transgenic C. elegans strain that models a mammalian disease or condition. Methods of using a system, e.g., for characterizing microbial strains of a mammalian microbiome and determining whether such microbial strains affect a mammalian disease or disorder.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.