scholarly journals Trypanosoma cruziInfection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Francisca Vorraro ◽  
Wafa H. K. Cabrera ◽  
Orlando G. Ribeiro ◽  
José Ricardo Jensen ◽  
Marcelo De Franco ◽  
...  

Trypanosoma cruziinfection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (HIII) or low (LIII) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRmax andHIIIwere resistant. The higher resistance ofHIIIas compared toLIIImice extended to higher infective doses and was correlated with enhanced production of IFN-γand nitric oxide production by peritoneal and lymph node cells, inHIIImales and females. We also analyzed the involvement of previously mapped Ab andT. cruziresponse QTL with the survival of Selection III mice toT. cruziinfections in a segregating backcross [F1(HIII×LIII)×LIII] population. An Ab production QTL marker mapping to mouse chromosome 1 (34.8 cM) significantly cosegregated with survival after acuteT. cruziinfections, indicating that this region also harbors genes whose alleles modulate resistance to acuteT. cruziinfection.

1990 ◽  
Vol 171 (6) ◽  
pp. 2115-2130 ◽  
Author(s):  
Y W Wong ◽  
A F Williams ◽  
S F Kingsmore ◽  
M F Seldin

The mouse BCM1 (OX45, Blast-1) antigen has been cDNA cloned and sequenced to provide data supporting the view that BCM1, LFA3, and CD2 constitute a subgroup within the Ig superfamily. Mouse BCM1 is widely expressed on leukocytes and is likely to be anchored to the cell surface by a glycosyl-phosphatidylinositol anchor, as is the case for rat and human BCM1 antigen. Genetic linkage studies by recombination and pulse field analysis showed the BCM1 locus (Bcm-1) to be on distal mouse chromosome 1 and to be linked within 1,600 kb to the locus for an ATPase alpha chain gene (Atpa-3). A similar relationship was established between the human BCM1 locus (BCM1) and ATP1A2, and other markers on chromosome 1q. Conservation of genomic organization within a segment of human chromosome 1q and mouse chromosome 1 was demonstrated. A similar situation is seen in the region of the CD2 and LFA3 genes between mouse chromosome 3 and human chromosome 1p. Furthermore, the CD2/LFA3 genes are linked within 580 kb to Atpa-1/ATP1A1 genes to provide a parallel situation to the linkage between Bcm-1/BCM1 and Atpa-3/ATP1A2 on chromosomes 1 (mouse) and 1q (human). Taken together, the data suggest duplication of a chromosome region including the precursors of the genes for BCM1, CD2, and LFA3, and the ATPase genes to give rise to the linkage groups now observed. The duplicated regions may have stayed together on chromosome 1 in the human (with the insertion of a centromere), while in the mouse, the genetic regions are proposed to have become dispersed in the formation of chromosomes 1 and 3. CD2 and LFA3 are more dissimilar in sequence than BCM1 and LFA3, and if the precursors of the CD2 and LFA3 loci formed before the proposed chromosome segment duplication, then a gene encoding a recognizer molecule for BCM1 may exist in linkage with Bcm-1/BCM1 on chromosome 1 (mouse) and 1q (human).


PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e25344 ◽  
Author(s):  
Zongji Lu ◽  
Zuobiao Yuan ◽  
Toru Miyoshi ◽  
Qian Wang ◽  
Zhiguang Su ◽  
...  

2021 ◽  
Vol 22 (4) ◽  
pp. 1959
Author(s):  
Marie-Sophie Girault ◽  
Sophie Dupuis ◽  
Côme Ialy-Radio ◽  
Laurence Stouvenel ◽  
Cécile Viollet ◽  
...  

Thanks to the analysis of an Interspecific Recombinant Congenic Strain (IRCS), we previously defined the Mafq1 quantitative trait locus as an interval on mouse Chromosome 1 associated with male hypofertility and ultrastructural abnormalities. We identified the Spermatogenesis associated protein 3 gene (Spata3 or Tsarg1) as a pertinent candidate within the Mafq1 locus and performed the CRISPR-Cas9 mediated complete deletion of the gene to investigate its function. Male mice deleted for Spata3 were normally fertile in vivo but exhibited a drastic reduction of efficiency in in vitro fertilization assays. Mobility parameters were normal but ultrastructural analyses revealed acrosome defects and an overabundance of lipids droplets in cytoplasmic remnants. The deletion of the Spata3 gene reproduces therefore partially the phenotype of the hypofertile IRCS strain.


2008 ◽  
Vol 7 (2) ◽  
pp. 214-223 ◽  
Author(s):  
J. R. Hofstetter ◽  
R. J. Hitzemann ◽  
J. K. Belknap ◽  
N. A. R. Walter ◽  
S. K. McWeeney ◽  
...  

2004 ◽  
Vol 17 (2) ◽  
pp. 215-220 ◽  
Author(s):  
Keith DiPetrillo ◽  
Shirng-Wern Tsaih ◽  
Susan Sheehan ◽  
Conrado Johns ◽  
Peter Kelmenson ◽  
...  

Hypertension is a complex phenotype induced by multiple environmental and genetic factors. Quantitative trait locus (QTL) analysis is a powerful method for identifying genomic regions underlying complex diseases. We conducted a QTL analysis of blood pressure in mice using 217 F2 progeny (males and females) from a cross between the normotensive C3H/HeJ and hypertensive SWR/J inbred strains. Our analysis identified significant QTL controlling blood pressure on chromosome 1 [Chr 1; Bpq8; peak 78 cM; 95% confidence interval 64–106 cM; logarithm of the odds ratio (LOD) 3.5; peak marker D1Mit105] and on Chr 16 ( Bpq9; peak 56 cM; 95% confidence interval 46–58 cM; LOD 3.6; peak marker D16Mit158). Bpq8 was previously identified in a cross between C57BL/6J and A/J mice, and we narrowed this QTL from 42 to 18 cM (95% confidence interval 68–86 cM) by combining the data from these crosses. By examining Bpq8 for regions where ancestral alleles were conserved among the high allele strains (C57BL/6J, SWR/J) and different from the low allele strains (A/J, C3H/HeJ), we identified a 2.3-cM region where the high allele strains shared a common haplotype. Bpq8 is concordant with known QTL in both rat and human, suggesting that the causal gene underlying Bpq8 may be conserved as a disease gene in human hypertension.


2005 ◽  
Vol 173 (4S) ◽  
pp. 137-137
Author(s):  
Michael M. Ohebshalom ◽  
Stella K. Maeng ◽  
Jie Chen ◽  
Dix P. Poppas ◽  
Diane Felsen

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