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TCATCA or TGATGA
Re: TCATCA or TGATGA
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Jan W. Koper, biochemist Dept. of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands, Elisabeth F.C. van Rossum, Steven W.J. Lamberts
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f.koper{at}erasmusmc.nl Jan W. Koper, et al.
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Dear Editor, With great interest we read the paper by Fleury et al. (Clin Chem 49(9), 1528, 2003), because our own interest is also in the field of glucocorticoid receptor polymorphisms. Having used a similar approach to these authors we have also identified this Bcl1 RFLP, resulting in a paper which is currently in press with Clinical Endocrinology (Oxf.). Upon careful reading of their paper, however, we observed that Fleury et al. state that the polymorphism is a TGATCA to TCATCA change, while we observed a TGATCA to TGATGA change. Of course we scrutinised our own sequence data, but found them to be correct. Further inspection of the Fleury data showed that the most probable cause of error is an inverted sequence autoradiogram (shown in their Fig. 1C). This sequence reads as TTAAAGAGATT(G/C)ATCAGCAGACA (polymorphism in parentheses). This sequence can only be made compatible with the sequence in NT_029289 (their point of origin), which is TGTCTGCTGAT(C)AATCTCTTTAA if one assumes that the autoradiogram has been flipped over horizontally (i.e. C should be G and A should be T). Another point in evidence is that the reported polymorphism (TGATCA to TCATCA) would concern the 643rd nucleotide of intron B (c.f. NT_029289)rather than the 647th (or 646th see legend to Fig. 1 and p. 1530, left column 7 lines above Table 1). The variation we found (TGATCA to TGATGA) is the 646th, and not the 647th nucleotide of intron B. This type of error is easily made, and we wish to emphasise that this response is only meant to avoid confusion in the literature about the genotype of a polymorphism that is currently of considerable scientific interest, and to establish that: 1. The glucocorticoid receptor Bcl1 polymorphism is caused by a C to G mutation of the 646th nucleotide of intron B of the GR-gene, destroying a Bcl1 restriction site (TGATCA to TGATGA). 2. By consequence, the minor allele, known as the 4.5 kb allele or the long allele in previous publications, should be referred to as the G- allele (with frequencies as those reported in the Fleury paper for what they call the C-allele, see also van Rossum et al. Clin. Endocrinol. (Oxf.) 2003, in press. Respectfully yours, Elisabeth F.C. Van Rossum Steven W.J. Lamberts Jan W. Koper |
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Maja Krajinovic, Assistant-Professor Centre de Recherche, Hôpital Ste-Justine, Département de Pédiatrie, Université de Montréal
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maja.krajinovic{at}umontreal.ca Maja Krajinovic
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Dear Editor, I would like to thank van Rossum et al. for their comments. There is, however, no difference between our report and the study of van Rossum et al. that will appear in Clinical Endocrinology. The misunderstanding arises because all our analyses, including primers for PCR and ASO as well as sequencing itself, are based on NT_029289 sequence which contains GR gene complement sequence. Therefore we reported the sequence of the antisense strand, whereas van Rossum et al., as can be seen from the text of the letter, reported the sequence of the sense strand for the Bcl I site. In our case the sequence is T(G)ATCA and in theirs it is TGAT(C)A. The mutation is C to G if the sense strand is reported and G to C if antisense strand is reported. The position of the mutation is in both cases the same, 646th nucleotide from intron B. This is stated in the text of our paper (page 1530, third paragraph, 15th line) as well as in the legend of figure 1(C) on page 1529. The number 647 refers to the position of the Bcl I site (again in regard to the complement sequence). Hoping that misunderstanding is clarified , I remain with best regards, Maja Krajinovic |
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