Provided for the first time in the present invention is a method for preparing a non-human primate somatic cell cloned animal, which method specifically comprises the steps of: (i) providing a reconstructed egg, wherein the egg comes from the non-human primate (ii) activating the reconstructed egg to form an activated reconstructed egg or activated reconstructed embryo formed by the reconstructed egg; (iii) reprogramming (a) the activated reconstructed egg or (b) embryonic cells of the activated reconstructed embryo to obtain a reprogrammed reconstructed egg or reprogrammed reconstructed embryo; and (iv) regenerating the reprogrammed reconstructed egg or reprogrammed reconstructed embryo to obtain the non-human primate somatic cell cloned animal. The method of the present invention can significantly improve the developmental capacity of nucleus-transplanted embryos in non-human primates (such as monkeys).

A non-human mammal and an offspring thereof, obtainable by a somatic cell nuclear transfer method using a nucleus of a CD4-positive T cell as a nuclear donor. The non-human mammal of the present invention surely and efficiently shows allergic reactions specific to various antigens that are shown to have associations with an immune allergic disease, such as mites and cedar pollens, so that the non-human mammal can be suitably used as the developmental models of allergic diseases for studies of various diseases by studying or pursuing possibilities of applications to the diseases.

The invention provides methods for reprogramming somatic cells to generate multipotent or pluripotent cells. Such methods are useful for a variety of purposes, including treating or preventing a medical condition in an individual. The invention further provides methods for identifying an agent that reprograms somatic cells to a less differentiated state.

A method of modulating some or all copies of a gene in a cell is provided including introducing into a cell one or more ribonucleic acid (RNA) sequences that comprise a portion that is complementary to all or a portion of each of the one or more target nucleic acid sequences, and a nucleic acid sequence that encodes a Cas protein and maintaining the cells under conditions in which the Cas protein is expressed and the Cas protein binds and modulates the one or more target nucleic acid sequences in the cell.

Disease model pigs produced by nuclear transplantation, disease model pigs exhibiting stable phenotypes and production methods thereof are provided. Chimeric pigs for producing disease model pigs exhibiting stable phenotypes, genital glands thereof, and germ cells thereof are also provided. A method for producing a genetically modified disease model pig, includes: (a) transplanting a nucleus of a genetically modified cell into cytoplasm of an egg; (b) developing an obtained clonal embryo in a womb of a female pig to obtain an offspring; and mating the obtained offspring or having the offspring undergo sexual reproduction to further obtain the genetically modified offspring as a disease model pig.

A method of modulating some or all copies of a gene in a cell is provided including introducing into a cell one or more ribonucleic acid (RNA) sequences that comprise a portion that is complementary to all or a portion of each of the one or more target nucleic acid sequences, and a nucleic acid sequence that encodes a Cas protein and maintaining the cells under conditions in which the Cas protein is expressed and the Cas protein binds and modulates the one or more target nucleic acid sequences in the cell.

A method of modulating some or all copies of a gene in a cell is provided including introducing into a cell one or more ribonucleic acid (RNA) sequences that comprise a portion that is complementary to all or a portion of each of the one or more target nucleic acid sequences, and a nucleic acid sequence that encodes a Cas protein and maintaining the cells under conditions in which the Cas protein is expressed and the Cas protein binds and modulates the one or more target nucleic acid sequences in the cell.

Manufacturing processes are described for biological replication of undifferentiated plant and animal cells and tissue in a weightless condition, including those systems used in current stem cell research and development and use of undifferentiated parenchyma in plants. Additionally, methods for adapting plants and animals to survive outside their native environments are described. In particular, undifferentiated cells from plants or animals are replicated under weightless conditions in which cell replication or proliferation is accelerated and sustained. Under such conditions, the undifferentiated cells can be forced to express sets of genes useful for survival in particular environmental conditions. In this manner, cells surviving prolonged exposure to specific environmental conditions can be selected for and cultivated to produce an organism adapted to that particular environment in an accelerated manner. Methods of identifying specific genes associated with adaptation of a plant or animal to a specific environment are also described.

The present invention provides novel methods for improving the efficiency of artificial activation of unfertilized mammalian oocytes by reducing the intracellular concentration of Zn.sup.2+ in the oocyte. The methods of the invention may additionally comprise a preceding step of increasing the intracellular concentration of Ca.sup.2+ in the oocyte prior to reduction of the intracellular Zn.sup.2+ concentration. The invention further provides unfertilized oocytes activated by the disclosed methods and viable mammalian animals produced from unfertilized oocytes activated by the disclosed methods.

Genomically modified livestock animals having a modification in one or more genes implicated in heart failure are provided. The animals provide models for various pathologies in heart failure including dilated cardiomyopathy and hypertrophic cardiomyopathy and can be used for investigation of new treatment methods including interventional devices, biologics and pharmaceuticals. The models can also be induced to develop metabolic syndrome (MetS) and are therefore amenable to further investigation of the confounding effects of MetS on the progress of heart failure.