Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  1
• Reference
  J:128536 Watanabe A, et al., Fabp7 maps to a quantitative trait locus for a schizophrenia endophenotype. PLoS Biol. 2007 Nov;5(11):e297
• ID
  MGI:3768793

Genes

Gene	Assay Type
Ppiq2	visible phenotype
D1Mit332	PCR amplified length variant
Asrq6	visible phenotype
D1Mit211	PCR amplified length variant

Notes

• Experiment
  Genetic loci associated with prepulse inhibition (PPI) deficiency, a biological marker of schizophrenia, were mapped in 1,010 animals from a (C57BL/6NCrlCrlj x C3H/HeNCrlCrlj)F2 intercross. Acoustic startle response (ASR) and ASR latency were also measured. Animals were phenotyped at 8- to 9-weeks of age. Parental strain C57BL/6NCrlCrlj displays higher PPI compared to parental strain C3H/HeNCrlCrlj. A panel of 80 polymorphic markers spaced approximately 20 cM apart was used for the genome scan.
  
  The strongest association to PPI mapped to 23 cM on mouse Chromosome 10 near Cdh23 with LOD=28.4. This locus accounts for 26.5% of the PPI variance and is named Ppiq1 (prepulse inhibition QTL 1). C57BL/6NCrlCrlj-derived alleles at Ppiq1 confer increased PPI values consistent with an additive or dominant mode of inheritance. Fine map analysis refined the Ppiq1 interval to a small region around Fabp7 (21.98 cM). A female-specific locus for PPI was identified between D10Mit175 (41.8 cM) and D10Mit261 (47 cM). Linkage to ASR latency mapped to 18.3 cM near D10Mit214 (LOD=4.3) and is named Latency4. This locus explains 2.8% of the phenotypic variance. C57BL/6NCrlCrlj-derived alleles at Latency4 confer increased ASR latency consistent with dominant or additive inheritance. Fabp7 is considered a candidate gene for Ppiq1 and Latency4. This gene is more highly expressed in the brains of C3H/HeNCrlCrlj animals compared to C57BL/6NCrlCrlj. In addition, Fabp7-deficient animals display reduced PPI and ASR latency.
  
  On mouse Chromosome 1 linkage to prepulse inhibition mapped to 41.8 cM near D1Mit332 with LOD=7.6. This locus explains 3.1% of the phenotypic variance and is named Ppiq2. C3H/HeNCrlCrlj-derived alleles at Ppiq2 confer increased PPI values with an additive mode of inheritance. Linkage to acoustic startle response mapped to 6 cM near D1Mit211 (LOD=3.5). This locus explains 1.7% of the ASR variance and is named Asrq6 (acoustic startle response QTL 6). C57BL/6NCrlCrlj-derived alleles at Asrq6 confer increased acoustic startle response values.
  
  Linkage to acoustic startle response mapped to 15.2 cM on mouse Chromosome 2 near D2Mit365 with LOD=4.7. This locus is named Asrq2 (acoustic startle response QTL 2). C3H/HeNCrlCrlj-derived alleles confer increased ASR values with an additive mode of inheritance. This locus explains 2.1% of the phenotypic variance.
  
  Linkage to prepulse inhibition mapped to 13.1 cM on mouse Chromosome 3 near D3Mit240 (LOD=4.1). This locus explains 1.7% of the phenotypic variance and is named Ppiq4 (prepulse inhibition QTL 4). C3H/HeNCrlCrlj-derived alleles at Ppiq4 confer increased PPI values.
  
  On mouse Chromosome 4 linkage to ASR latency mapped to 40.1 cM near D4Mit166 (LOD=8.7) and is named Latency1. C57BL/6NCrlCrlj-derived alleles confer increased ASR latency. This locus explains 8.5% of the phenotypic variance.
  
  Linkage to acoustic startle response mapped to 0.5 cM on mouse Chromosome 7 near D7Mit21 (LOD=3.9). This locus is named Asrq5. C3H/HeNCrlCrlj-derived alleles at Asrq5 confer increasedASR value with an additive mode of inheritance. This locus explains 2.1% of the ASR variance. Linkage to prepulse inhibition mapped to 37.9 cM near D7Mit301 (LOD=5) and is named Ppiq3. C3H/HeNCrlCrlj-derived alleles at Ppiq3 confer increased PPI values with additive inheritance. This locus explains 2.2% of the PPI variance.
  
  On mouse Chromosome 11 linkage to prepulse inhibition mapped to 31.7 cM near D11Mit242 (LOD=3.9). This locus explains 1.6% of the PPI variance and is named Ppiq5. C57BL/6NCrlCrlj-derived alleles at Ppiq5 confer increased PPI values with dominant inheritance. Linkage to acoustic startle response mapped to 35.7 cM, also near D11Mit242 (LOD=7.6). This locus is named Asrq1. C3H/HeNCrlCrlj-derived alleles confer increased ASR with an additive mode of inheritance. Asrq1 explains 3.6% of the phenotypic variance.
  
  Linkage to acoustic startle response mapped to 42.7 cM on mouse Chromosome 12 near D12Mit214 (LOD=4.1). This locus is named Asrq4 (acoustic startle response QTL 4). C57BL/6NCrlCrlj-derived alleles at Asrq4 confer increased ASR values with additive inheritance. Asrq4 explains 1.8% of the phenotypic variance.
  
  On mouse Chromosome 13 linkage to ASR latency mapped to 21.9 cM near D13Mit103 (LOD=4.7). This locus is named Latency3. C3H/HeNCrlCrlj-derived alleles confer increased ASR latency with additive inheritance. Latency3 explains 4.2% of the phenotypic variance. Linkage to prepulse inhibition mapped to 41.8 cM near D13Mit224 (LOD=3.8). This locus explains 1.6% of the PPI variance and is named Ppiq6. C3H/HeNCrlCrlj-derived alleles confer increased PPI values consistent with an additive or dominant mode of inheritance. Ofcc1 and Dtnbp1 (23 cM) map to the Ppiq6 95% confidence interval. Both genes are considered candidate genes for schizophrenia susceptibility in humans.
  
  Linkage to ASR latency mapped to 60.5 cM on mouse Chromosome 15 near D15Mit107 (LOD=5.2) and is named Latency2. This locus explains 4.7% of the phenotypic variance. C57BL/6NCrlCrlj-derived alleles confer increased ASRlatency with additive inheritance.
  
  Linkage to acoustic startle response mapped to 47.6 cM on mouse Chromosome 16 near D16Mit76 (LOD=8.7). This locus is named Asrq3 and explains 8.5% of the ASR variance. C3H/HeNCrlCrlj-derived alleles at Asrq3 confer increased ASR values with additive inheritance.