A Predominant Role for Parenchymal c-Jun Amino Terminal Kinase (JNK) in the Regulation of Systemic Insulin Sensitivity (original) (raw)
Figure 3
Generation of JNK1-deficient radiation chimeras using bone marrow transplantation.
The extent of engraftment of the transplanted cells in WT recipients after bone marrow transplantation was determined using genomic DNA isolated from whole blood and quantified with PCR-based allele distribution (A and B). Genomic DNA harvested from tail confirmed the presence of only the recipient genotype (A) while genomic DNA from liver, subcutaneous fat, and epididymal fat tissues (C) confirmed engraftment of donor (_Jnk1_-deficient) cells in WT recipients. Genomic DNA isolated from blood was quantified as in panel A except in the Jnk1−/− recipient groups (D and E). Genomic DNA isolated from the liver, subcutaneous fat, and epididymal fat tissues (F) of Jnk1−/− recipients confirmed the genotype and engraftment, respectively. At 8 weeks of age, all WT (G) and Jnk1−/− (H) recipient chimeras transplanted with WT or Jnk1−/− bone marrow cells were placed on high fat diet and body weights were monitored for the duration of experiments.