[Federal Register Volume 68, Number 221 (Monday, November 17, 2003)]
[Notices]
[Pages 64903-64904]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-28657]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, HHS.

ACTION: Notice.

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SUMMARY: The invention listed below is owned by an agency of the U.S. 
Government and is available for licensing in the U.S. in accordance 
with 35 U.S.C. 207 to achieve expeditious commercialization of results 
of federally-funded research and development. Foreign patent 
applications are filed on selected inventions to extend market coverage

[[Page 64904]]

for companies and may also be available for licensing.

ADDRESSES: Licensing information and copies of the U.S. patent 
application listed below may be obtained by writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: 301-496-7057; fax: 301-402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent application.

High Efficiency Single Stranded Homologous Recombination in Host Cells 
Deficient for Mismatch Repair

Donald L. Court et al. (NCI); PCT Application No. PCT/US03/14657 filed 
09 May 2003 (DHHS Reference No. E-038-2003/0-PCT-01); Licensing 
Contact: Norbert Pontzer; 301/435-5502; [email protected].
    Homologous recombination is the process of exchanging DNA between 
two molecules through regions of identical sequence. Homologous 
recombination provides an alternative to using restriction 
endonucleases and ligases for producing recombinant DNA. However, the 
background level of homologous recombination in E. coli is very low 
even with long homology arms. Previous improvements have provided 
methods of using bacterophage lambda Red recombination functions to 
greatly increase the recombination frequency of endogenous single- and 
double-stranded DNA with relatively short homology arms. This type of 
genetic engineering has been named ``recombineering,'' a convenient 
term to describe homology-dependent, recombination-mediated, genetic 
engineering. Recombination with endogenous linear single-stranded DNA 
(ssDNA) is likely to occur by annealing with transiently single-
stranded regions of the chromosome such as the replication fork. We 
show that only the Beta component of the Red function is required for 
this activity. (Published PCT Application WO00/21449; Nat. Rev. Genet. 
2001, 2:769-779.)
    When the ssDNA used for recombineering introduces change(s) near 
the DNA replication fork, the change(s) may trigger mismatch repair 
(MMR), which in turn can reduce the level of recombination. In the 
present invention, altering MMR function achieves a 10-to 100-fold 
increase in Red recombination. This increase raises the number of 
recombinants to 25 to 30 percent of treated cells surviving 
electroporation of the oligo. Methods of transiently inhibiting MMR and 
bacterial strains deficient for the production of MMR genes are also 
provided. (Annu. Rev. Genet. 2002, 36:361-88.)

    Dated: November 7, 2003.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 03-28657 Filed 11-14-03; 8:45 am]
BILLING CODE 4140-01-P