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The Joshua Lederberg Papers

Letter from Roger Y. Stanier to Joshua Lederberg pdf (115,831 Bytes) transcript of pdf
Letter from Roger Y. Stanier to Joshua Lederberg
Item is handwritten.
Number of Image Pages:
2 (115,831 Bytes)
1950-06-02 (June 2, 1950)
Stanier, Roger Y.
Lederberg, Joshua
Courtesy of Joshua Lederberg.
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Lederberg Grouping: Correspondence B
Box Number: 8
Folder Number: 64
Unique Identifier:
Accession Number:
Document Type:
Letters (correspondence)
Physical Condition:
Series: Correspondence, 1935-2002
SubSeries: 1947-1953
Folder: Stanier, Roger Y.
June 2
Dear Joshua - -
I enquired at the housing bureau today. Nothing has been found for you yet, but the woman there is confident that there will be no difficulty, so don't worry.
Am very busy getting things cleared up so that I can leave by June 14 for Seattle. However, I wanted to tell you of some fascinating observations by Klein in adaptations in Ps. putiefacies[?]. Wild type P.p. grows well in sucrose and maltose but not in glucose or fructose. Last year, Klein showed that it gives rise to spontaneous glucose-[ . . . ] mutants, the biochemical basis of the mutation apparently being the ability of the mutants to produce an (adaptive) gluconkinase.
The picture then became:
The fate of the free fructose [ . . . ] is till unclear (no fructokinase in the cells).
Recently, he stated to study maltose breakdown (also adaptive) and discovered to our joint amazement that maltose-grown wild-type cells are simultaneously adapted to both maltose and glucose. It could be argued, of course, that growth[?] on maltose had selected for the glucose mutant, but this eliminated a) by showing that maltose-grown cells, transferred to glucose, showed the typical 4-5 day lag before growth occurred that signalizes[?] selection
of the rare glucose mutants and b) that wild type cells grown in broth and then adapted to maltose in resting cell suspension could oxidize glucose and maltose at the same rate thereafter. This finding of course wreaks our simple picture of the biochemical basis for the glucose mutation. We have two hypotheses : a) the Kleinian - - that w.t. cells are impenetrable to free glucose, so that only glucose formed internally (e.g. in maltose breakdown) can initiate adaptation. On this basis, the mutation would be nothing[?] only a change in permeability b) the Stanierian - - that for some reason in w.t. cells induction of glucokinase formation by the substrate in blocked, but induction by maltose can occur. This would make the glucose mutation a change in the inductive mechanism, rather than a change in permeability.
Any ideas on this? The Kleinian hypothesis in untenable, I think.
Best wishes
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