Werner syndrome is a human progeroid syndrome caused by mutations at the We
rner helicase locus (WRN). Progeroid features and diseases associated with
aging (including arteriosclerosis) do not become apparent until after puber
ty. We entertained two alternative hypotheses to explain the post-pubertal
onset: 1) WRN expression is induced at the time of puberty, its earlier fun
ctions being satisfied by another member of that family of helicases; and 2
) it is expressed at all ages, but the phenotype of deficiency becomes appa
rent only after puberty. We report initial experiments consistent with the
second hypothesis. Steady-state levels of WRN mRNA in aortic tissues were d
etermined by semiquantitative reverse transcription-polymerase chain reacti
on. WRN mRNA was detectable as early as 49 days of gestation (the earliest
available material). There was no statistically significant change in these
levels between fetal and adult tissues. Thr presence of the WRN protein in
fetal aorta was confirmed by Western analysis. This rules out the possibil
ity that Werner syndrome phenotypes manifest after the puberty because of p
eripubertal induction of WRN expression. (C) 1999 Elsevier Science Inc. All
rights reserved.