Disclosed are methods for increasing the fertilization rate of an oocyte in a granulosa cell-oocyte complex, and/or the success rate of in-vitro fertilization by using mitochondrial therapies. Also disclosed are methods of identifying compounds for fertility treatment.

Disclosed are methods for increasing the fertilization rate of an oocyte in a granulosa cell-oocyte complex, and/or the success rate of in-vitro fertilization by using mitochondrial therapies. Also disclosed are methods of identifying compounds for fertility treatment.

The present invention provides methods and compostions to improve the efficiency of somatic cell nuclear transfer (SCNT). There is increasing evidence that the epigenetic state of donor nuclei has a significant impact on potential of nuclear transfer embryos to develop into blastocysts, from which pluripotent stem cells are derived. Strategic application of histone agents, capable of altering epigenetic state such as methylation, allows zygotic activation and robust blastocyst generation.

The present invention provides methods and compostions to improve the efficiency of somatic cell nuclear transfer (SCNT). There is increasing evidence that the epigenetic state of donor nuclei has a significant impact on potential of nuclear transfer embryos to develop into blastocysts, from which pluripotent stem cells are derived. Strategic application of histone agents, capable of altering epigenetic state such as methylation, allows zygotic activation and robust blastocyst generation.

The present disclosure provides a promoter having at least the core components of a duck retinoic acid-inducible gene I (RIG-I) promoter, as well as expression constructs having the duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein), and recombinant host cells containing the duck RIG-I promoter, e.g., in such expression constructs. The present disclosure also provide animals genetically modified to have a gene encoding a duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein, such as a duck RIG-I protein).

The present disclosure provides a promoter having at least the core components of a duck retinoic acid-inducible gene I (RIG-I) promoter, as well as expression constructs having the duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein), and recombinant host cells containing the duck RIG-I promoter, e.g., in such expression constructs. The present disclosure also provide animals genetically modified to have a gene encoding a duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein, such as a duck RIG-I protein).

An object of the present invention is to provide a method of conveniently producing a genetically modified non-human mammal with high efficiency using a CRISPR-Cas9 system and particularly a production method whereby gene knock-in can be achieved with high efficiency regardless of the gene size. The method of producing a genetically modified non-human mammal comprises introducing a Cas9 protein, a crRNA fragment comprising a nucleotide sequence complementary to a target DNA region, and a tracrRNA fragment into a non-human mammalian oocyte to genetically modify the target DNA.

An object of the present invention is to provide a method of conveniently producing a genetically modified non-human mammal with high efficiency using a CRISPR-Cas9 system and particularly a production method whereby gene knock-in can be achieved with high efficiency regardless of the gene size. The method of producing a genetically modified non-human mammal comprises introducing a Cas9 protein, a crRNA fragment comprising a nucleotide sequence complementary to a target DNA region, and a tracrRNA fragment into a non-human mammalian oocyte to genetically modify the target DNA.

The present disclosure relates to using CRISPR-based methods to perform gene editing to correct frame shift mutations in alleles with detectable phenotypes, and to correct aneuploidies.

The present disclosure relates to using CRISPR-based methods to perform gene editing to correct frame shift mutations in alleles with detectable phenotypes, and to correct aneuploidies.