A detailed letter with extensive commentary on a forthcoming article authored by Stern.
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5 (490,629 Bytes)
1937-06-27 (June 27, 1937)
Original Repository: American Philosophical Society. Library. Curt Stern Papers
Reproduced with permission of the Curt Stern Papers, American Philosophical Society.
Medical Subject Headings (MeSH):
Crossing Over, Genetic
Breakage-Fusion-Bridge: The University of Missouri, 1936-1941
Box Number: 3
Folder Number: 3
June 27, 1937.
I am returning the paper which you sent to me. Since you stated you were leaving July 1, I have had to hurry to get it back
to you in time and have not given it the amount of thought I should like to have. However, I have some comments which I should
like to make.
The facts about the Wx - wx case of dimorphism of the pollen and its staining reaction is common knowledge to maize geneticists,
i.e., when the reaction con be noted. From our experience the starch begins to appear shortly after the first division of
the microspore (about 5 days after meiosis) but the staining reaction with iodine is not good until just before the pollen
is ready to shed. The wx gene is not a good case since wx is located close to the spindle fiber attachment region on the
short arm of chromosome 9 and probably is segregated in the first meiotic mitosis. The tetrads in higher plants are of two
kinds with regard to division of the cytoplasm. In some (monocots mainly) the first mitosis is followed by cell wall formation.
In other plats (dicots mainly) the two meiotic mitoses take place in a common cytoplasm. Wall formation does not occur until
after the two nuclear divisions are completed. Datura has this form of tetrad production while maize has the former type.
The case Miss Clark is working on, which she has described to you, is quite relevant. At the end of the first meiotic mitosis
10 chromosomes (full set) are in each cell although not all in one nucleus. In the second division these nuclei form one
to several spindles all in one cytoplasmic mass of each dyad. Wall formation takes place producing four or more cells depending
upon the orientation of the spindles in the second division dyads. In each cell there are from one to several nuclei with
one or more chromosomes in each. About five days elapse between the end of the meiotic divisions and the first division in
the microspore in which growth and differentiation of the spores take place. What takes place during this period is a direct
expression of the chromosome content of the nuclei. The spores with deficient chromosome complements do not develop normally
(cytoplasm degenerates or nuclei appear degenerate) although they came from cytoplasm exposed during the second meiotic mitoses
to the full genomic complement on the basis of release of genes at this period. The spores with a full genomic complement,
although in separate nuclei, develop normally. In this case, the effect of the chromosome complement in the "resting
nucleus" is immediately expressed. If genes were being released into the cytoplasm during division all the spores, regardless
of their compositions, should progress normally until after the first division in the spore, unless the genes have been unequally
distributed in the cytoplasm.
[Beginning of handwritten section]
If genes were released during division of the nucleus how would they be distributed to the cytoplasm of the two daughter cells.
Cell wall formation takes place very rapidly in plants. It starts during ana phase and is completed by early telophase.
If genes were released here, some mechanisms for distributions in the cytoplasm before wall formation or division of cytoplasm
of adjacent cells, would have to be [ . . . ]. We do not get any spreading of genic activity thru walls in the ear of the
Cl gene which produces a [ . . . ] where [ . . . ] colorless rap. I have tested this with a ring chromosomes with [ . . .
] where, the ring chromosome lost from the nucleus during somatic division [ . . . ] develop. There is a spread of the Bm2
gene [ . . . ] produces a brown cell wall). In a cell with [ . . . ] which is adjacent to Bm2 cell, the wall of the brown
cell immediately adjacent to the Bm2 cell is Rm2 or a very [ . . . ]. The Bm2 effect [ . . . ] the run cell not only on the
[ . . . ] wall.
It seems to me release of genes at mitosis introduces another problem. You have not mentioned this in your paper.
[End of handwritten section]
There are other cases in maize that can be used. We have an interchange between chromosome 6 (with the nucleolus organizer)
and chromosome 5. In the heterozygous condition it produces the following figure:
Crossing over occurs in the marked region in from 50 - 75% of the sporocytes (depending upon environmental conditions). As
a result of such crossing-over, each telophase I nucleus has a full genomic complement (when such crossing-over occurs, segregation
of homologous spindle fiber regions occurs always at I). At TI, the chromosome constitutions after such crossing-over are:
A full genomic complement is present in each nucleus, although not balanced. If genes are released during nuclear divisions,
deficient and normal chromosome carrying spores should develop at similar rates. This, however, does not occur. Spores with
the full genomic complement develop much faster. Spores with deficient chromosome complements develop much slower. I have
not figured out the rates of differential development of each type of spore in this particular interchange, where crossing-over
has been measured, but it is a common practice to look for these types in others of different ages. The first spores to go
through divisions are normal chromosome-carrying spores, the last to go through the first division in the spore are the deficient
chromosome carrying spores. I can look more carefully for timing and let you know.
I think the spore development cases in maize could be used quite effectively if the right set-ups were chosen. I have several
cases involving inversions and deficiencies which could be easily used. I will briefly outline a deficiency case which can
be done easily. We hate plants with a deficiency in chromosome 5 which is covered by a ring chromosome. Plants heterozygous
for this deficiency and ring have one normal chromosome 5, one deficient chromosome 5 and a ring chromosome. The deficient
and the normal chromosome 5 pair and segregate normally at meiosis.
The ring chromosome divides at I and gets into practically every TI nucleus. In II, the ring chromosome does not divide again
but wanders to one or the other pole, sometimes being included in the nucleus and sometimes not. All the necessary genes
are present in the TI nuclei but the TII nuclei are hyperploid, hypoploid and normal. The hypoploid pollen is practically
empty of starch. I may be able to find a dimorphism of the spores before the first division and relate it to the deficient
and full genome carrying complements (the hyperploid complement is known to have practically the same division rate as the
normal and need not be a factor). Since at metaphase II, the full genomic compliment is present in all cells, there should
be no spore dimorphism related to full and deficient genomic carriers on the basis of release of genes at nuclear divisions.
If such is found, the constitution of the "resting nucleus" is the determining factor in differentiation.
I have spent some time describing the possibilities of spores in maize since I think they can be decisive cases. They can
give better evidence than the wx gene. The case of endosperm constitution in Jone's paper is not particularly good in
my estimation since he has not proven the number of nuclei in his endosperm cells. Some of his large cells may be multinucleate
(I strongly suspect).
Is it obvious in Ustilago that the spores 1,2 and 3,4 are sister cells? In some forms the divisions are not strictly linear
but the spindles are placed as follows:
In this case, adjacent spores are not sister spores.
The case of Pascher appears to me to be the strongest but I wish it were better analyzed from a genetic point of view.
It seems to me that the geneticists have assumed that the genic activity of the nucleus takes place from the "resting
nucleus" without, as you point out, the necessary evidence. I don't think our apparent evidence at the present time
is very decisive. The geneticists have considered the "resting nucleus" as the actively functioning organ bar so
long, based on differentiation, dedifferentiation and wound responses (in plants) that they have not been alert to the evidence
when it did appear and have not pointed it out as such but have taken it for granted.
You don't mention the paper of Berril and Huskins in the American Naturalist 70, (May-June) 1936, entitled "The Resting
nucleus". You may have seen it and found it not to your point.
About publishing the paper - A short paper pointing out the need of decisive evidence is not out of order. A question for
a title is quite appropriate under the circumstances. There should be some response to such a question. Would you publish
in the Am. Nat.? It is an appropriate place for such an article.
I was pleased to learn you were to make a trip home. I hope it will be successful. Miss Clark tells me you are expecting
another F1 - or shouldn't I know? I'll try to get up and see you after your return - sometime toward the end of August.
Last summer was so difficult I had no time off all summer and was even three weeks late getting to my new job.
My best to you and Evelyn.
[Remainder of document handwritten]
I am sorry this is so hastily written and co[ . . . ], but there may be something in it you might wish to know, provided I
have made it anywhere near clear enough and I have my doubts!