Technical Problem The purpose of the present invention is to provide a method which enables sex selection in a non-human animal, and enables a coming individual to have no recombination gene, and a transgenic non-human animal giving birth to individuals of only one sex, which is used in the method.

Solution to Problem The present disclosure relates to a male transgenic non-human animal in which one of an X chromosome and a Y chromosome comprises an exogenous embryonic death induction gene operatively connected to a drug-responsive promoter. The present disclosure also includes a method for producing a male transgenic non-human animal for sex selection.

Provided is an arthropod male germline gene expression system suitable for conditional expression of an effector gene in an Arthropod male germline. The system comprises a first expression unit comprising an effector gene and a promoter therefor operably linked thereto; and a second expression unit. Said second unit comprises a coding sequence for a transcription factor and an upstream regulatory element operably linked thereto, the transcription factor being capable of acting upon the promoter in the first expression unit to drive expression of the effector gene. The upstream regulatory element includes a promoter for the transcription factor; and a 5 UTR adjacent a start site for the transcription factor coding sequence. The upstream regulatory element driving sufficient expression of the transcription factor such that the transcription factor protein in turn drives transcription of the effector gene before meiosis. Also provided are uses of the system for instance in methods of biocontrol and quality control.

It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.

Methods of disrupting germ cell migration and development in a fish embryo by inducing targeted expression of Sdf-1a or Lif and disruption of the Sdf-1a gradient or a Lif signaling pathway in the fish embryo have been developed. Plasmid constructs containing a gene encoding Sdf-1a or Lif and a gene encoding a signaling sequence for targeted expression of Sdf-1a or Lif have been generated. The plasmids will be administered to a fish or a population of fish to reproductively sterilize the population with efficacy of up to 100%. Transgenic fish of this invention are reproductively incompetent of genetically contaminating a wild fish population.

Non-human animals comprising a reverse-conditional null endogenous lysosomal storage disease gene and methods of making such non-human animals are provided. Also provided are methods of using the non-human animals for assessing reversibility of a phenotype of the lysosomal storage disease or for determining an optimal timeframe for treatment of a phenotype of the lysosomal storage disease.

The invention provides inducible promoter systems and their components incorporating components of a tetracycline operon. By coordinating expression of different transcriptional units in these systems as a result of selection of promoters and/or linking the units into the same DNA molecule, these systems can achieve higher levels of expression of coding segments of interest, increased differential levels of expression between on- and off-states, and/or greater responsiveness to inducing agents than conventional systems.

Disclosed herein are methods and compositions useful in treating a neuropathy caused by a CNTNAP1 mutation. Transgenic animal models and cell lines are disclosed for the study of neuropathies caused by a CNTNAP1 mutation. Methods of screening and identifying active agents for the treatment of neuropathies caused by a CNTNAP1 mutation are also provided.

Disclosed is a method for preparing T cells for adoptive T cell therapy by contacting a population of activated T cells with an AT-rich interaction domain 1A (Aridla) inhibitor. Also disclosed is a kit, a population of T cells or engineered T cells produced by the method and use of the same in adoptive T cell therapy and the treatment of cancer.

Aspects of the disclosure provide compositions and methods for reversible expression of a target gene. In some aspects, the disclosure provides nucleic acids comprising multiple pairs of recombinase sites, each pair having first and second members flanking an inverted expression cassette encoding a target gene.

Disclosed are compositions, methods, and kits for modifying DNA within cells as well as compositions and methods for modifying gene expression in a cell. In particular, the invention generally relates to compositions, methods, and kits for DNA editing using single-stranded DNA. Compositions and methods for modifying gene expression using artificial microRNAs (amiRNA) are also contemplated.