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© 1993 Oxford University Press

OTHER

An embryonic-like methylation pattern of classical satellite DNA is observed in ICF syndrome

M. Jeanpierre*,, C. Turleau1, A. Aurias2, M. Prieur2, F. Ledeist3, A. Fischer3 and E. Viegas-Pequignot1

Unité INSERM U129 and Service de Biochimie Génétique, ICGM CHU Cochin 24 rue du Faubourg Saint-Jacques 75014, Paris 1U173 INSERM, 147 rue de Sèvres, Hopital Necker-Enfants-malades Paris 2UA 620 CNRS, Institut Curie Section de Biologie, rue d'Ulm, Paris 3U132 INSERM, 147 rue de Sèvres, Hopital Necker-Enfants malades Paris, France

* To whom correspondence should be addressed

Received February 3, 1993; Revised March 31, 1993; Accepted March 31, 1993

ICF syndrome has been described as the association of variable immunodeficiency, facial anomalies and centromeric heterochromatin instability. Since the chromosome rearrangements seen in cells of ICF patients are reminiscent of the chromosomal changes induced by the undermethylating agent 5-azacytidine in the late S-phase, we have analyzed the methylation pattern of satellite sequences in four patients. These sequences are almost completely methylated in normal leukocyte DNA. When ICF DNA was tested with methylsensitive enzymes, several classical satellite families, but not alphoid sequences, showed a very low level of methylcytosine in leukocyte DNA, with an abnormal pattern compared to the normal germinal and extraembryonic methylation profile. The methylation deficiency affects classical satellite families built from distinct unit sequences but located in the same chromosomal region. This observation may have important implications for the mechanism of chromosomal rearrangements.


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