Agronomy and Horticulture, Department of

 

Date of this Version

Summer 7-2012

Document Type

Thesis

Citation

Portions published as: Hepburn, N.J., Schmidt, D.W. and Mower, J.P. (2012) Loss of two introns from the Magnolia tripetala mitochondrial cox2 gene implicates horizontal gene transfer and gene conversion as a novel mechanism of intron loss. Molecular Biology and Evolution, in press.

Comments

A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science, Major: Agronomy, Under the Supervision of Professor Jeffrey P. Mower. Lincoln, Nebraska: July, 2012

Copyright 2012 Nancy Jimenez Hepburn

Abstract

It has been 35 years since the discovery of introns. Although fundamental aspects of their function and evolutionary origins have been widely studied, the mechanisms of intron loss are still an unresolved evolutionary mystery. Previously proposed mechanisms of intron loss include exonization, random genomic deletion and retroprocessing. The mitochondrial genomes of land plants have been characterized by widespread intron loss. In angiosperms, two introns located in the cox2 gene display a particularly variable intron distribution, indicating frequent loss. We took advantage of the frequent intron loss from cox2 to investigate the possible mechanisms of loss from this gene. The first study focused on Maganolia tripetala, a species that contains two cox2 gene copies that differ in intron content. Transcriptional and phylogenetic analyses indicated that the edit site distribution was not consistent with the retroprocessing model. Instead, we showed that the loss of two group II introns from the mitochondrial cox2 gene of Magnolia tripetala was mediated by a novel mechanism involving horizontal gene transfer and gene conversion (HGT-GC). In a broader study involving all angiosperms, we found no support for intron loss via exonization and random genomic deletion. We also did not find strong evidence supporting retroprocessing as the sole mechanism of intron loss. Our overall findings suggest that HGT-GC or an unidentified mechanism plays a larger role in the loss of introns than previously recognized.

Adviser: Jeffrey P. Mower

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