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Originally published as Genetics Published Articles Ahead of Print on September 2, 2005.
Genetics, Vol. 171, 2151-2155, December 2005, Copyright © 2005
doi:10.1534/genetics.105.048066
The Small Introns of Antisense Genes Are Better Explained by Selection for Rapid Transcription Than by "Genomic Design"
Jianjun Chen*,1,
Miao Sun*,
Janet D. Rowley* and
Laurence D. Hurst
* Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, Illinois 60637 and Department of Biology and Biochemistry, University of Bath, Somerset BA2 7AY, United Kingdom
1 Corresponding author: Section of Hematology/Oncology, Department of Medicine, University of Chicago, 5841 S. Maryland Ave., MC 2115, Chicago, IL 60637.
E-mail: jchen{at}medicine.bsd.uchicago.edu
ABSTRACT
Several models have been proposed to explain why expression parameters of a gene might be related to the size of the gene's introns. These include the idea that an energetic cost of transcription should favor smaller introns in highly expressed genes (the "economy selection" argument) and that tissue-specific genes reside in genomic locations with complex chromatin level control requiring large amounts of noncoding DNA (the "genomic design" hypothesis). We recently proposed a modification of the economy model arguing that, for some genes, the time that expression takes is more important than the energetic cost, such that some weakly but rapidly expressed genes might also have small introns. We suggested that antisense genes might be such a class and showed that the data appear to be consistent with this. We now reexamine this model to ask (a) whether the effects described were owing solely to the fact that antisense genes are often noncoding RNA and (b) whether we can confidently reject the "genomic design" model as an explanation for the facts. We show that the effects are not specific to noncoding RNAs and that the predictions of the "genomic design" model for the most part are not upheld.
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