Transposons are mobile genetic elements that have the potential to cause mutations as a result of different aspects of their life cycle. Because most of these mutations are detrimental and due to a selfish life cycle seemingly aiming at increasing their numbers, transposons have been regarded as "junk" DNA that contributes no evolutionary function to the host organism. In this thesis, I argue that although most of the transposon-induced mutations are detrimental, some may lead to benefits for the host and become adaptive. I discuss recent evidence from the literature that points to several mechanisms by which transposons and transposon activity may lead to the diversification of host genes and gene functions. I also provide evidence that transposons have inserted in the 5' flanking region of the gene coding for maize and teosinte auxin-binding protein 1 (Abp1). These transposons do not change the structure of the Abp1 transcripts but may modulate Abp1 gene expression quantitatively. In addition, I document the first case outside of oncogenic retroviruses, of a retrotransposon (called Bs1) that transduced portions from three different maize genes. I show that the Bs1-associated transduction events resulted in the formation of one uninterrupted open reading frame that is both transcribed and translated in reproductive tissues. I suggest that, such as in the case of Bs1, gene transduction by retroelements may be a general mechanism for the evolution of new hybrid genes by the shuffling of host sequences. I conclude that transposons are better regarded as means for the generation of gene and genomic diversity. Natural selection will favor and fix adaptive variants whereas detrimental mutations are likely to be purged out of the population.

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