Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.

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Abstract
The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5.