Jobes1b QTL Detail

Summary

• Symbol
  Jobes1b
• Name
  juvenile obesity 1b
• Synonyms
  jObes1, jObes1

• Feature Type
  QTL
• IDs
  MGI:5911135
• Candidate Genes
  1 Gene

Location &
Maps

• Sequence Map
  Chr3:36534149-36904149 bp

  From MGI annotation of GRCm39
  

• View this region in JBrowse
  

• Genome Browsers
  Ensembl | UCSC | NCBI

• Genetic Map
  Chromosome 3, cM position of peak correlated region/marker: Syntenic
• Mapping Data
  2 experiments

Mutations,
Alleles, and
Phenotypes

• Phenotype Summary
  1 phenotype reference
  

• All Mutations and Alleles
  2
• QTL
  2
• Find Mice (IMSR)
  0 strains or lines available

References

• Summaries
  All 2

  Phenotypes 1
• Earliest
  J:243037 Neuschl C, et al., A unique genetic defect on chromosome 3 is responsible for juvenile obesity in the Berlin Fat Mouse. Int J Obes (Lond). 2010 Dec;34(12):1706-14
• Latest
  J:242866 Arends D, et al., Fine mapping a major obesity locus (jObes1) using a Berlin Fat Mouse x B6N advanced intercross population. Int J Obes (Lond). 2016 Nov;40(11):1784-1788

Candidate Genes for Jobes1b:

Gene	Genome Location (GRCm39)	Reference	QTL Note
Bbs7	Chr3:36627291-36667626 (-)	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.