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Lack of Imprinting of Three Human Cyclin-Dependent Kinase Inhibitor Genes¹

Departments of Molecular Biology & Genetics [G. J. C., A. P. F.], Medicine [J. S. T., B-A. R., J-Y. L., A. P. F.], and Oncology [A. P. F.], Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Genomic imprinting is an epigenetic modification in the germline leading to parental allele-specific gene expression in somatic cells. We have previously found that imprinted genes can be abnormally expressed or silenced in tumors and that the cyclin-dependent kinase inhibitor (CKI) CDKN1C (p57^KIP2) is normally imprinted, with preferential expression of the maternal allele. Here we analyze the imprinting status of three additional CKIs, the abnormal expression and/or chromosomal localization of which has been implicated in human malignancy: CDKN1A, CDKN1B, and CDKN2C. Allele-specific expression was examined by reverse transcription-PCR, using primers that span transcribed polymorphisms as well as exon/intron boundaries, to distinguish cDNA products from genomic DNA. Biallelic expression was observed for all three genes in both fetal and adult tissues. Thus, genomic imprinting is not a generalized feature of CKIs.

¹ This work was supported by NIH Grant CA65145 (to A. P. F.) and Biochemistry and Cellular & Molecular Biology Training Grant GM07445 (to G. J. C.).

² To whom requests for reprints should be addressed, at Johns Hopkins University School of Medicine, Ross 1064, 720 Rutland Avenue, Baltimore, MD 21205. Phone: (410) 614-3489; Fax: (410) 614-9819.

Received 12/13/96. Accepted 1/ 6/97.