By use of newly developed subcongenic strains of mice from a parental B6.129-Il10-/- knockout/congenic strain, we have narrowed the critical region for a new behavioral QTL, called Emo4, for open-field activity to a segment of Chromosome 1 between Erbb4 (68.4Mb) and B3gnt7 (86.2 Mb). We have also uncovered an additional QTL governing repetitive beam breaks in the open field. This QTL, called Reb1, maps to the interval between Asb1 (91.4 Mb) and NM_172851 (100.0 Mb) and is one of the first QTLs mapped for this type of behavior. Genome-wide microarray expression analyses were then undertaken to help to identify candidate genes that may be the cause of these genetic differences in open-field performance. In this effort, we analyzed global gene expression differences in the amygdalae by use of Affymetrix GeneChips between B6, B6.129-Il10-/-, and B6.129R4. Several probe sets representing target Chr 1 genes were found that showed significantly differential expression in the subcongenic and congenic strains. Several candidate genes have been identified. One of these regions coincides with an homologous region in humans that has been associated with autism, a disease whose symptoms include repetitive actions. This study illustrates that the use of congenic strains combined with global gene expression analyses can produce a list of viable candidates. It further shows that caution should be observed when analyzing the effects of knockout/congenic strains because many of the gene expression differences in these comparisons could not be attributable to the ablated Il10 gene but rather to passenger gene effects.
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http://dx.doi.org/10.1007/s00335-005-0107-y | DOI Listing |
Exp Anim
December 2024
Division of Experimental Animals, Graduate School of Medicine, Nagoya University.
Streptozotocin (STZ) is widely used as a pancreatic beta-cell toxin to induce experimental diabetes in rodents. Strain-dependent variations in STZ-induced diabetes susceptibility have been reported in mice. Differences in STZ-induced diabetes susceptibility are putatively related to pancreatic beta-cell fragility via DNA damage response.
View Article and Find Full Text PDFInfect Genet Evol
January 2025
Laboratory of Laboratory Animal Science and Medicine, Department of Applied Veterinary Sciences, Graduate School of Veterinary Medicine, N18 W9, Kita-Ku, Sapporo, Hokkaido 060-0819, Japan.
Alveolar echinococcosis is a zoonosis caused by the larval stage of Echinococcus multilocularis. In previous studies, QTL analysis using C57BL/6 N (B6) and DBA/2 (D2) which differ in susceptibility suggested the presence of genes on chromosome 1 that control protoscolex development. In this study, we constructed several congenic mice with different chromosome 1 regions substituted to confirm the presence of responsible genes and to narrow down the regions where the responsible genes exist.
View Article and Find Full Text PDFHorm Metab Res
October 2024
Department of Pathology, State University of Campinas (UNICAMP), Campinas, Brazil.
Objective: To determine the downstream effects on ovarian function and immune cell differentiation in the ovary and uterus using a model in which RGS2 was knocked out specifically in CD4+ T cells.
Design: Laboratory based experiments with female mice.
Animals: Female congenic (fully backcrossed) and non-congenic (mixed strain) mice with CD4 T cell-specific RGS2 knockout.
Biology (Basel)
October 2024
Division of Clinical Chemistry and Pharmacology (KKF), Department of Biomedical and Clinical Sciences (BKV), Linköping University, 581 83 Linköping, Sweden.
To demonstrate causation or/and assess pathogenic mechanisms of environment-induced autoimmunity, various animal models that mimic the characteristics of the human autoimmune diseases need to be developed. Experimental studies in mice reveal the genetic factors that contribute to autoimmune diseases. Here, the immune response of two mouse strains congenic for non-H-2 genes, A.
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