Rick C. M.
Dr. Burdick's note on the make-up of chromosome 7 calls for a reply, although I have very little new data to shed light on the situation. The expression of wt is variable, and one is sometimes hard pressed in deciding where to draw the line between a maninifestation of wt/wt and environmentally-induced curling of the leaves. In some lines segregation seems to be well-defined; in others, not. In view of these difficulties with wt, I certainly think that the final word has not yet been spoken, but I am no more convinced by the evidence from linkage than I am by the trisomic data. I would also like to call attention to the following points:
(1) The linkage tests have given a wide array of values, covering a range of 20 units from independent segregation down to the value of 30 reported by Fogle and Currence. Also, a point not brought out by Burdick is that MacArthur, who did the original work on this combination, concluded that j and vt were independent on the basis of a value of .475 +- .01. Variation in tomato linkage values have been reported before, but nothing yet has reached this extraordinary fluctation. Something out of the ordinary is happening here, and I wonder if it is not a developmental correlation between j and wt, which is subject to environmental control and not linkage. I would also be interested in knowing whether the same wt gene has been used throughout, or whether possibly the wiltiness in Tiny Tim used by Fogle and Curence might be conditioned by some gene other than wt.
(2) The linkage group proposed by Burdick covers a length of 145 units: n 30 wt 40 Cf\3 16 i 32 a 23 f 4 bi. Now, whether these genes are on chromosome 7 or not, it is certain that they are not located on the two longest chromosomes of the tomato set. Furthermore the maximum number of xta. observed per bivalent is two. One wonders how such a long linkage map could be built up with so little crossingover. If a comparison could be drawn with chromosome 2 having one of the longest arms of the set, even with the 15 genes that have been assigned to it, its total map distance is only 77 units and the last 16 units to Lc rest on rather
(30 Recalling what I said above concerning wt, I would like to point out that if the trisomic data were at fault, then the error lies in the tests between wt and chromosome 7, and not between a and the same chromosome. I take this stand because, not only is the classification of a unmistakable, but also independent trisomic tests were obtained between j and f and chromosome 7. If groups V and X are ultimately proved to belong on the same chromosome it is not chromosome 7.
Finally, it seems to me that the proof will rest on linkage tests with Cf\3 or other markers that might lie at closer intervals to the genes in question.
As to the hypothetical lf gene, which Burdick reincarnates, I doubt if anyone can be certain the jointless and leafy effects are independent. If they are independent, then why are they both invariably associated with j\1, j\2, mc, and two other mutants mentioned by Sawant and me in TGC 5:26? If we insist on a separate gene for leafiness associated with j\1, we will have to do the same with the four other genes to be consistent in our reasoning. Then why not five tightly linked genes for the jointlessness, leafiness, defective calyx, proliferation of inflorescences, and elongate fruits and pedicels of j\2, or three for the gray color, drooping leaves and dwarf habit of wd, or three for the variant leaf shape, short internodes, and defective flowers of cl\2, etc.? Finally, are each of these combinations situated in proximal chromatic regions and therefore not subject to crossingover? I realize that the recent emphasis on pseudoalleles has stimulated a lot of thinking about manifestations of closely linked genes, but I find it simpler to think of the tomato genes associated with multiple effects as single pleiotropic genes until the effects have been separated by crossingover.