The results of 563 crosses of Mutator stocks that had been made in the years 1973 through the winter crop of 1980-81 have been summarized. Of these crosses 85 (13.1%) of the Mutator parents had lost mutator activity. If one line that had an exceptionally high loss rate (24.4%) is excluded, the rate becomes 11.8%. It has been shown (MGCNL 51:36, 1977) that not all apparent losses are real. Occasionally, the sample of 50 outcross plants used to score for the presence of Mutator activity will not include a plant carrying a mutant, as a result of sampling error. If larger samples of outcrossed plants are tested such "sampling error" Mu-loss events can be recognized. A limited test of 13 apparent Mu-Iosses revealed that 5 were due to sampling error. This is not a large enough sample to establish a frequency for such misclassifications but it does serve to demonstrate that they are not insignificant. Because of this uncertainty, it is difficult to estimate the true Mu-loss rate. The value of 13.1 % determined for 563 crosses is surely an overestimate because most of these Mu losses were not tested further to determine whether or not they were true losses. The observation that one line, mentioned above, has a 24.4% loss rate suggests that different stocks may differ with respect to this phenomenon. In light of the uncertainties, we have suggested a value of 10% as the best estimate of the loss frequency.

To test whether Mu-Ioss plants had some system (genetic or otherwise) that in some manner inhibited transposition of the Mu1 transposon, active Mutator plants were crossed as males to first generation Mu-loss stocks. The F1's were crossed to standards and the resulting progeny were scored for presence of new mutants (Table 1).

It does not appear that the Mu-loss parent contributed anything that induced the inactivation of Mutator. Some of the above outcrossed plants (i.e. stand. x (Mu-loss/Mu)) were again outcrossed as males to determine if there was a delayed effect of the original Mu-loss parent on the activity of Mu, or if there was any evidence of Mendelian segregation for the Mu phenotype (Table 2).

Only three 1980-81 families were tested. Two of them (i.e. 80-81-1530 and 1532) appear to be low Mu-Ioss lines, although the numbers are not large enough for determining the frequency of Mu-loss with any accuracy. Most of the outcrosses from family 80-81-1531, however, did not segregate for new mutants, indicating that their 80-81-1531 parents had lost Mutator activity. The level of Mutator activity in the parent of the 80-81-1531 family can not be determined with certainty. At most, the parent appears to be a weak mutator, which may account for the high Mu loss frequency in the next generation.

It is obvious that Mutator activity frequently can be retained after crossing active Mutator plants with those that have lost Mu activity. The one instance (involving family 80-81-1531) where there might be an effect of the Mu-loss condition on Mu may have nothing to do with the Mu-loss parent but may just represent an ordinary Mu loss phenomenon. Thus there is no convincing evidence that Mu-loss stocks possess an inhibitor for Mu1 transposition.

Table 1. Mutator activity in Mu-loss/Mu F1 plants.

Table 2. Mutator activity in plants of the first outcross generation of Mu-loss/Mu plants i.e., stand/ (Mu-loss plants x Mu).

Donald S. Robertson
 
 

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