POSTSCRIPT

Correspondence

Low-frequency protamine 1 gene transversions c.102GT and c.–107GC do not correlate with male infertility.

E Kichine¹, S Msaidie^1,2, A D Bokilo², A Ducourneau^1,2, A Navarro¹, N Levy^1,3, P Terriou⁴, P Collignon⁵, G Boetsch², J Chiaroni⁶, M J Mitchell¹

¹ Inserm U.910, Faculté de Médecine, 13385 Marseille, France
² Anthropologie Biologique UMR 6578, Faculté de Médecine, 13385 Marseille, France
³ Département de Génétique Médicale, Hopital d’enfants de la Timone, 13385 Marseille, France
⁴ Institut de Médecine de la Reproduction, 13008 Marseille, France
⁵ Service de Génétique, Centre Hospitalier de Toulon, 83056 Toulon, France
⁶ Etablissement Français du Sang Alpes-Mediterranée, 13005 Marseille, France

Correspondence to:
Dr M J Mitchell, Inserm U.910, Faculté de médecine, 13385 Marseille, France; mitchell@medecine.univ-mrs.fr

The first 150 words of the full text of this article appear below.

Iguchi et al,¹ and Ravel et al.² have proposed that, in the heterozygous state, the c.102GT and the c.-107GC transversions in the protamine 1 gene (PRM1), could be causes of human male infertility. Deleterious mutations in one allele of the human PRM1 gene are reasonably expected to have a dominant negative effect on male fertility, because in the mouse, germ cells carrying one null Prm1 allele do not produce viable gametes.³ In human PRM1 studies,^{1 2} however, several infertile men carried one of the two transversions, evoking the possibility of founder effects and therefore efficient transmission. To explore this apparent paradox, we screened 1195 infertile and control men for these two transversions, and conclude that neither has a significant effect on male fertility.

Iguchi et al originally described the 102T variant in 3 heterozygotes out of 30 infertile men with a normal sperm count . . . [Full text of this article]

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