The implications of the presence of introns in genes of bacteria and bacterial viruses are still emerging. In particular, the origin and evolution of splicing mechanisms in the bacteria are particularly controversial. Although rare, introns are widely distributed among bacteria and their phages. Genes encoding endonucleases, that reside within the introns, may be responsible for intron spread to unoccupied sites in other genomes, or their transposition to sites in different genes. Intron endonucleases and related proteins outside introns may be responsible for selective propagation of nearby genes, contributing to the dynamics of bacterial and phage populations. We will explore whether (1) the self-splicing of phage introns may be regulated by the cellular growth rate; (2) if enzymatic tRNA splicing evolved from group I self-splicing in bacteria; (3) the apparently independent spread of an intron and its endonuclease gene within a family of Gram positive bacteriophages and their hosts; (4) the role of a large family of intron endonuclease-related phage proteins in competition between genes of closely related phages; (5) a possible novel role for an intron endonuclease in autoregulation of its own transcription. Some of the phages we will investigate infect pathogenic bacteria. If the introns in the phage are also present in essential genes of their pathogenic hosts, this may lead to design of chemotherapeutic agents that block splicing. The long-term objectives of the project are to learn about how splicing evolved, and how introns and their associated proteins contribute to the evolution of bacteria and their viruses.
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