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Am J Physiol Lung Cell Mol Physiol 279: L326-L332, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 2, L326-L332, August 2000

Quantitative trait locus mapping of genes regulating pulmonary PKC activity and PKC-alpha content

Lori D. Dwyer-Nield1, Beverly Paigen2, Stephanie E. Porter1, and Alvin M. Malkinson1

1 Department of Pharmaceutical Sciences and University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, Colorado 80262; and 2 Jackson Laboratory, Bar Harbor, Maine 04609

Strain A/J mice, which are predisposed to experimentally induced asthma and adenocarcinoma, have the lowest pulmonary protein kinase (PK) C activity and content among 22 inbred mouse strains. PKC in neonatal A/J mice is similar to that in other strains, so this difference reflects strain-dependent postnatal regulation. PKC activity is 60% higher in C57BL/6J (B6) than in A/J lungs, and the protein and mRNA concentrations of PKC-alpha , the major pulmonary PKC isozyme, are two- to threefold higher in B6 mice. These differences result from more than a single gene as assessed in F1, F2, and backcross progeny of B6 and A/J parents. Quantitative trait locus (QTL) analysis of 23 A×B and B×A recombinant inbred strains derived from B6 and A/J progenitors indicates a major locus regulating lung PKC-alpha content that maps near the Pkcalpha structural gene on chromosome 11 (D11MIT333; likelihood ratio statistic = 12.5) and a major locus controlling PKC activity that maps on chromosome 3 (D3MIT19; likelihood ratio statistic = 15.4). The chromosome 11 QTL responsible for low PKC-alpha content falls within QTLs for susceptibilities to lung tumorigenesis and ozone-induced toxicity.

protein kinase C; inbred mouse strains; developmental regulation; genetic mapping; lung tumor susceptibility


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