Abstract
Life expectancy among species varies widely and is obviously a genetically-controlled characteristic. The genetic control of life span among different strains of the same species also varies significantly (1) and is a subject of considerable scientific interest. An early radiation-effects study reported that genetically-controlled life span was shortened by radiation-induced mutations with slight dominant effects (2). The conclusions of this early report have been discredited by substantial conflicting experimental evidence (3, 4), and reduction in life expectancy has since been shown to be a poor indicator of radiation-induced genetic injury (4). The theory that radiation-induced multiple mutations with minor effects accumulate to cause significant decrements to such characteristics as life span, activity, and radiation resistance is consistent with present knowledge of the genetic control of these characteristics. However, if a significant effect on these characteristics can be attributed to a single gene locus, it becomes necessary to take another look at the reliability of these end points as measures of accumulated genetic injury suggested by the multiple minor mutation theory. The results of an investigation on the possible influence of a single gene locus on life span and its relationship to activity and radiation resistance are described below.
Experimental Methods. Two lines of strain RFM mice from the same parent pair were found to have different radiation resistance characteristics (5). Mice in the two lines were serotyped by the hemagglutination method of Gorer and Mikulska (6). Both H-2k and H-2f serotypes were segregating in each line, one line being predominantly H-2k and the other predominantly H-2f. Two sublines were developed within each of the two lines so that each line had an H-2k and an H-2f subline. Radiation resistance characteristics were shown to segregate with the H-2 serotype, with H-2k mice showing more resistance to protracted gamma-ray exposure than the H-2f mice (7).
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