A Mouse for All Reasons

@article{Collins2007AMF,
  title={A Mouse for All Reasons},
  author={Francis S. Collins and Janet Rossant and Wolfgang Wurst},
  journal={Cell},
  year={2007},
  volume={128},
  pages={9-13}
}
Three major mouse knockout programs are underway worldwide, working together to mutate all protein-encoding genes in the mouse using a combination of gene trapping and gene targeting in mouse embryonic stem (ES) cells. Although the current emphasis is on production of this valuable resource, there are significant efforts to facilitate program coordination, to enhance the availability of this resource, and to plan for future efforts in mouse genetics research. 
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A New Partner for the International Knockout Mouse Consortium
TLDR
A recent Commentary in Cell outlined the plans of three major programs in the US, Canada, and Europe to mutate all protein-encoding genes in the mouse using a combination of gene targeting and gene trapping in mouse embryonic stem (ES) cells. Expand
Bi-allelic gene targeting in mouse embryonic stem cells.
TLDR
Inducible homozygous cells described here provide a precisely controlled experimental system to study gene function in a model cell and present a method for conditional ablation of genes in ES cells using vectors and targeted clones from the EUCOMM and KOMP conditional resources. Expand
Trends in large-scale mouse mutagenesis: from genetics to functional genomics
  • Y. Gondo
  • Biology, Medicine
  • Nature Reviews Genetics
  • 2008
TLDR
The origins and rationale of large-scale mouse mutagenesis programmes are traced to develop a fundamental research infrastructure for mammalian functional genomics and to produce human disease models. Expand
Dual RMCE for efficient re-engineering of mouse mutant alleles
TLDR
dRMCE is a scalable, flexible tool to introduce tags, reporters and mutant coding regions into an endogenous locus of interest in an easy and highly efficient manner. Expand
A conditional knockout resource for the genome-wide study of mouse gene function
TLDR
High-throughput genome engineering highlighted by this study is broadly applicable to rat and human stem cells and provides a foundation for future genome-wide efforts aimed at deciphering the function of all genes encoded by the mammalian genome. Expand
The mammalian gene function resource: the international knockout mouse consortium
TLDR
The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research. Expand
Identifying essential genes in mouse development via an ENU-based forward genetic approach.
TLDR
An efficient and non-biased, N-ethyl-N-nitrosourea (ENU)-based forward genetic approach in mouse provides a unique tool for the identification of genes essential for development and adult physiology via ENU-based mutagenesis, which has become a powerful tool in deciphering gene functions. Expand
A review of current large‐scale mouse knockout efforts
TLDR
The knockout mouse project (KOMP) and the international gene trap consortium (IGTC) were initiated to create convenient resources for scientific research worldwide and knock out all the mouse genes. Expand
Towards better mouse models: enhanced genotypes, systemic phenotyping and envirotype modelling
The mouse is the leading mammalian model organism for basic genetic research and for studying human diseases. Coordinated international projects are currently in progress to generate a comprehensive… Expand
Mouse mutants and phenotypes: accessing information for the study of mammalian gene function.
TLDR
Methods to quickly obtain information on what mutant ES cells and mice are available are described, including recombinase driver lines for the generation of conditional mutants, to access genetic and phenotypic data that identify mouse models for specific human diseases. Expand
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References

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TLDR
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TLDR
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TLDR
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As part of the course at York each person is given the task of creating a character to present to the rest of the group. About ten weeks are allowed for its growth but hardly any of the preparation… Expand
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