PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of narLink to Publisher's site
 
Nucleic Acids Res. Apr 25, 1985; 13(8): 2855–2867.
PMCID: PMC341199

A beta zero-thalassemic beta-globin RNA that is labile in bone marrow cells is relatively stable in HeLa cells.

Abstract

We have shown previously that a beta-globin RNA-deficient beta zero-thalassemia is caused by a single base-pair deletion in codon 44 of the human beta-globin gene1. The lack of beta-globin RNA in erythroid cells of these affected individuals is due to extreme beta-globin RNA instability (t 1/2 = 30 min)2. We have further investigated the mechanism of this extreme lability by transiently expressing the beta zero-thalassemic allele in HeLa cells and assaying the stability of the beta-globin RNA that is produced. Surprisingly, the beta zero-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 beta-globin genes. In HeLa cells, beta-globin RNAs harboring deletions in and around the translation initiation codon accumulate to steady-state levels that are similar to the level of normal beta-globin RNA.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (2.1M), or click on a page image below to browse page by page.

Images in this article

Click on the image to see a larger version.

Articles from Nucleic Acids Research are provided here courtesy of Oxford University Press