| Human Disease | Mouse Models | ||||
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IDs
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IDs
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early conceptus |
embryo ectoderm |
embryo endoderm |
embryo mesoderm |
embryo mesenchyme |
extraembryonic component |
alimentary system |
auditory system |
branchial arches |
cardiovascular system |
connective tissue |
endocrine system |
exocrine system |
hemolymphoid system |
integumental system |
limbs |
liver and biliary system |
musculoskeletal system |
nervous system |
olfactory system |
reproductive system |
respiratory system |
urinary system |
visual system |
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| Transcription Start Site | Location | Distance from Gene 5'-end |
| Tssr33043 | Chr3:36667638-36667649 (-) | -18 bp |
| Tssr33042 | Chr3:36667610-36667620 (-) | 11 bp |
| Tssr33041 | Chr3:36667567-36667578 (-) | 53 bp |
| Tssr33040 | Chr3:36667519-36667546 (-) | 93 bp |
| Tssr33039 | Chr3:36667488-36667516 (-) | 124 bp |
| Tssr33038 | Chr3:36653560-36653589 (-) | 14,051 bp |
| QTL | Genetic Location* | Genome Location (GRCm39) | Reference | QTL Note |
| Jobes1b | Chr3, syntenic | Chr3:36534149-36904149 | J:242866 | The Berlin Fat Mouse Inbred line 860 (BFMI860) is a model for juvenile obesity. Previously, a recessive major effect locus (jObes1) on chromosome 3 between 34 and 44 Mb had been found to be responsible for 39% of the variance of total fat mass at 10 weeks in a (BFMI860/Hber x C57BL/6NCrl) F2 population. The aim of the current study was to fine map the jObes1 locus. Curator Note: The previous study mapping jObes1 was J:243037; the jObes1 QTL identified as mapping the total fat mass locus was assigned official nomenclature and is now Jobes1b. An advanced intercross line (AIL) was generated from the initial F2 mapping population. Three hundred and forty-four male mice of generation 28, Hber:B6N,BFMI860-G28, were excessively phenotyped and genotyped using the MegaMuga mouse chip containing 22,164 informative single-nucleotide polymorphisms. The high mapping resolution of the AIL reduced the confidence interval for Jobes1b from 10 to 0.37 Mb between 36.48 and 36.85 Mb (GRCm38). The region was highly significantly (LOD score >50) associated with total fat mass starting at puberty (6 weeks). Male homozygous carriers of the Jobes1b BFMI allele had 3 g more fat than the other genotypes. Surprisingly, the genotype class showed lower body mass until weaning at 3 weeks (LOD = 3.2). The mapped interval contained four genes [Table 2]. Bbs7, the most likely candidate gene that also caused obesity in complementation tests was differentially expressed in all tissues examined, whereas the neighboring cyclin A2 (Ccna2) gene showed differential expression in gonadal adipose tissue. Many of the small effect QTLs for juvenile obesity that were found at the genome-wide 5% significance level in the initial F2 mapping population as reported by Neuschl et al. [J:243037] could not be confirmed in this study. Possibly the QTLs reported for the F2 population were either spurious or their effects got lost because epistatic interaction or joined effects of genes in close proximity were interrupted through the many recombination events that occurred during the pedigree history of the advanced intercross population until generation 28. |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/10/2024 MGI 6.24 |
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