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Nucleic Acids Research, 1985, Vol. 13, No. 8 2855-2867
© 1985

Articles

A ß°-thalassemic ß-globin RNA that is labile in bone marrow cells is relatively stable in HeLa cells

Lynne E. Maquat and Alan J. Kinniburgh

Department of Human Genetics, Roswell Park Memorial Institute, New York State Department of Health 666 Elm Street, Buffalo, NY 14263, USA

Received November 9, 1984. Revised March 18, 1985. Accepted March 18, 1985.

We have shown previously that a ß-globin RNA-deficient ß°-thalassemia is caused by a single base-pair deletion in codon 44 of the human ß-globin gene1. The lack of ß-globin RNA in erythroid cells of these affected individuals is due to extreme ß-globin RNA instability (t1/2=30 min)2 We have further investigated the mechanism of this extreme lability by transiently expressing the ß°-thalassemic allele in HeLa cells and assaying the stability of the ß-globin RNA that is produced. Surprisingly, the ß°-thalassemic RNA is much more stable in HeLa cells than in bone marrow cells. Apparently, developing erythroid cells have a mechanism for turning over this thalassemic RNA while cervical carcinoma cells do not. We also have assayed the stability of RNA derived from in vitro-mutagenized ß-globin genes. In HeLa cells, ß-globin RNAs harboring deletions in and around the translation initiation codon accumulate to steady-state levels that are similar to the level of normal ß-globin RNA.


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