A reply: the human proacrosin gene

Abstract

Vazquez-Levin et al. have published, in this edition of your journal, a paper on the molecular cloning, sequencing and restriction mapping of the genomic sequence encoding human proacrosin [I]. The gene was isolated by using our human proacrosin cDNA probe [2] which we sent to Dr Gordon in 1990. The results obtained by the authors confirm the nucleotide sequence and genomic organization of the proacrosin gene which we published in 1990 [3]. Vazquez-Levin et al. report two differences between their nucleotide sequence and ours, namely in 22 bases of intron 1 and in the localisation of a cytosine residue in exons 3 and 4. We would like to comment on these differences. 1. Vazquez-Levin et al. [l] report in the abstract of their paper that the 500 bases sequenced distal to the initial 54 bases at the 5’ end of intron 1 shows no similarity to our published sequence [3]. Such a conclusion is not justified because we have published only 76 bases of the 5’ end of intron 1. We have obtained this 76-bp sequence by sequencing the 1.2-kb PstIEcoRI genomic fragment containing exon 1, intron 1 and exon 2 from both ends (Fig. 1 in [3]). Therefore, we believe the explanation that an inversion is the reason for the 22-bp difference between our sequence and that of Vazquez-Levin et al. to be unlikely. 2. Vazquez-Levin et al. state that the boundaries of the third intron of the human proacrosin gene differed such that a cytosine residue reported by us in exon 3 [3] was found to be the first base of exon 4. This situation is true in the proacrosin gene of mouse [4], rat [5] and boar (unpublished results), but not in the human proacrosin gene. To exclude possible sequencing errors, we confirmed the results in the human proacrosin gene several times and the cytosine residue was always found in exon 3. Vazquez-Levin et al. [l] report that they have sequenced more than 500 bases of the promoter region of the human