34 MUTATIONS 



Lederberg: Which would, if so, ah'eady constitute a difference. You 

 must know about that, Bentley. 



Glass: We have never been able to demonstrate any antigens on 

 white cells. 



Atwood: By fluorescent technique or anything else? 



Glass: We haven't used fluorescent methods. 



Cotterman: You mean by agglutination? 



Glass: Mixed co-agglutination tests. 



Cotterman: What type of reagent did you use? 



Glass: Anti-A, anti-B, and anti-H. 



Cotterman: Phytoagglutinins, as well as sera? 



Glass. Kodani did use Ulex agglutinins (19). 



Lederberg: These, presumably, would be the lymphocytes and 

 polymorphs, but not the monocytes. Monocytes certainly do have 

 surface antigen, don't they? 



Glass: I don't believe that Kodani was able to make a distinction 

 between types of white cells. 



Auerbach: Wasn't this rise also observed for the Ai, which is still 

 antigenic? 



Atwood: Yes. It is not stable for the A2. 



Auerbach: But could it not be some phenocopy effect? About a year 

 ago, there was an article in Nature (14), in which somebody working 

 with leukemic patients found that during the leukemic attack he got 

 A2 in an Ai patient. It went away when the man was treated. When 

 he had a recurrence, the same change in the blood group took 

 place. Might the introduction of the P^- have a similar effect? 



Atwood: We could speak of the penetrance of the gene at the cell 

 level and say that it has 99.9 per cent penetrance, which is why we 

 see 1 in 1000 non-A cells. This is a terrrible idea, but it might be 

 true. 



Lederberg: Why terrible? 



Atwood: The actual value of penetrance now has to be explained. 

 Why should it be of the order of 1 in 1000 or 1 in 10,000? 



Neel: Kim, aren't you the person who suggested variation in the 

 number of reactive sites on the red cell as an explanation of non- 

 penetrance? 



Atwood: Yes, that you might have a distribution of sites that is 

 characteristic of that site system. Cells in the tail end of the distribu- 

 tion could have too few sites to be agglutinable. 



Lederberg: Can you relate the time of the P^^ decay with the time 

 of appearance of these aberrant cells? Just when in the history of a 



