PCR-analyzed microsatellites for the inbred mouse strain 129/Sv, the strain most commonly used in gene knockout technology

1996 ◽  
Vol 7 (8) ◽  
pp. 603-605 ◽  
Author(s):  
C. Matouk ◽  
D. Gosselin ◽  
D. Malo ◽  
E. Skamene ◽  
D. Radzioch
Keyword(s):  
Mouse Strain ◽  
Gene Knockout ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Knockout Technology ◽  
Gene Knockout Technology

scholarly journals Role for Neutrophils in Host Immune Responses and Genetic Factors That Modulate Resistance to Salmonella enterica Serovar Typhimurium in the Inbred Mouse Strain SPRET/Ei

2010 ◽  
Vol 78 (9) ◽  
pp. 3848-3860 ◽  
Author(s):  
Lien Dejager ◽  
Iris Pinheiro ◽  
Pieter Bogaert ◽  
Liesbeth Huys ◽  
Claude Libert
Keyword(s):  
Mouse Strain ◽  
Salmonella Enterica ◽  
Genetic Factors ◽  
Inbred Mouse ◽  
Critical Role ◽  
Inbred Mouse Strain ◽  
Natural Resistance ◽  
Host Bacterium ◽  
A Genome ◽  
Serovar Typhimurium

ABSTRACT Infection with Salmonella enterica serovar Typhimurium is a complex disease in which the host-bacterium interactions are strongly influenced by genetic factors of the host. We demonstrate that SPRET/Ei, an inbred mouse strain derived from Mus spretus, is resistant to S. Typhimurium infections. The kinetics of bacterial proliferation, as well as histological examinations of tissue sections, suggest that SPRET/Ei mice can control bacterial multiplication and spreading despite significant attenuation of the cytokine response. The resistance of SPRET/Ei mice to S. Typhimurium infection is associated with increased leukocyte counts in the circulation and enhanced neutrophil influx into the peritoneum during the course of infection. A critical role of neutrophils was confirmed by neutrophil depletion: neutropenic SPRET/Ei mice were sensitive to infection with S. Typhimurium and showed much higher bacterial loads. To identify genes that modulate the natural resistance of SPRET/Ei mice to S. Typhimurium infection, we performed a genome-wide study using an interspecific backcross between C3H/HeN and SPRET/Ei mice. The results of this analysis demonstrate that at least two loci, located on chromosomes 6 and 11, affect survival following lethal infection with S. Typhimurium. These two loci contain several interesting candidate genes which may have important implications for the search for genetic factors controlling Salmonella infections in humans and for our understanding of complex host-pathogen interactions in general.

Using the inbred mouse strain SPRET/EiJ to provide novel insights in inflammation and infection research

2018 ◽  
Vol 29 (7-8) ◽  
pp. 585-592
Author(s):  
Steven Timmermans ◽  
Jolien Souffriau ◽  
Jolien Vandewalle ◽  
Lise Van Wyngene ◽  
Kelly Van Looveren ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain

scholarly journals Impaired Pavlovian fear extinction is a common phenotype across genetic lineages of the 129 inbred mouse strain

2009 ◽  
Vol 8 (8) ◽  
pp. 744-752 ◽  
Author(s):  
M. Camp ◽  
M. Norcross ◽  
N. Whittle ◽  
M. Feyder ◽  
W. D’Hanis ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Fear Extinction ◽  
Genetic Lineages ◽  
Common Phenotype

scholarly journals Genetic differences between substrains of the inbred mouse strain 101 and designation of a new strain 102

1985 ◽  
Vol 46 (3) ◽  
pp. 349-352 ◽  
Author(s):  
John D. West ◽  
Mary F. Lyon ◽  
Josephine Peters ◽  
Paul B. Selby
Keyword(s):  
Inbred Strain ◽  
Genetic Polymorphisms ◽  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Genetic Differences ◽  
The Other ◽  
Genetic Loci ◽  
Genetic Contamination

SUMMARYGenetic polymorphisms revealed two distinct substrains of the inbred strain 101. One group included substrains 101*/Rl, 101/H and 101/HOxe; the other group comprised 101/El and 101/Sl. The two groups differed at 5 of the 8 genetic loci tested. The accompanying paper (Evans, Burtenshaw & Adler, 1985) shows that the two groups also differ for several chromosome polymorphisms. We suggest that genetic contamination occurred during the derivation of 101/El from 101/Rl and was already present in 101/El when 101/Sl was produced from this substrain. We further propose that these substrains be renamed 102/El and 102/Sl respectively.

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