Survey of Genomes - Campylobacter jejuni
Ka Shing Allan So from the 2019 Hiram College Genetics course introduces us to the largest bacterial cause of food-related gastrointestinal infections - Campylobacter jejuni.
Welcome to Genomics Revolution. This is Ka Shing Allan So from the 2019 Hiram College Genetics course hosting this episode on the genome of Campylobacter jejuni, or C. jejuni.
C. jejuni falls under the Campylobacteraceae family, and the Campylobacter genus. Campylobacter jejuni was discovered by Theodor Escherich. In 1886, Escherich was studying stool specimens and large intestinal mucous correlated to diarrhea in kittens and in neonates. He published his result in “The Intestinal Bacteria of the Infant and Their Relation to the Physiology of Digestion”. Escherich would grow cultures from infant stool samples and he successfully identified 19 different bacteria including Campylobacter jejuni.
C. jejuni is one of the highest causes of food poisoning in the United States. In 2011, the CDC predicted over 845,000 C. jejuni-related illness each year.
One particular strain of C. jejuni, strain NCTC11168, has a circular chromosome of only 1.6 million bp and two additional plasmids of 35 thousand bp each. Due to how small the C. jejuni genome is, it was genetically modified into CjCas9 for more efficient CRISPR-Cas9. Up to 1,654 proteins are predicted to be encoded by the C. jejuni genome.
Something very interesting about the C. jejuni genome is how few repeated sequences it has with only four repeated sequences consisting of three copies of the ribosomal RNA operon which are 6 thousand bp in size and three duplicates of the open reading frame. Repeated sequences are important as they could suggest highly preserved sequence, for example, the ribosomal RNA operon seen here. Repeated sequences are also important as tandem aid in mutations. A lack of repeated sequence suggests either slow mutation, or mutation through a different method.
Which brings us to another interesting fact about C. jejuni, its inability to perform DNA repair. C. jejuni does mutate, in fact some genomic regions show as much as three times more variation when compared with another organism like E. coli under similar conditions. This rapid phase of variation suggest that C. jejuni was unable to repair it’s own DNA. DNA sequencing found that the direct repair genes ada and phr, among other repair genes, were no where to be found in the C. jejuni sequence. C. jejuni mutates, simply by not repairing their DNA!!!
Another interesting fact about the C. jejuni genome is how few operons or cluster of genes there are. Some sets of proteins are still encoded by the same operons, for example the ribosomal protein operons. However, up to 617 families of genes are scatter through out the genome. For example, the Tyrosine, Aspartic Acid, and Glutamine synthesis genes can be found scattered randomly. While it seems to make it difficult to study, on the contrary, it allows us to focus on how important the genes that are grouped together must be. For example, the lipopolysaccharide gene clusters must have be involved in the synthesis of surface structures.
Isn’t C. jejuni interesting. Thank you for listening.
Bacon, D. J., Alm, R. A., Burr, D. H., Hu, L., Kopecko, D. J., Ewing, C. P., . . . Guerry, P. (2000). Involvement of a Plasmid in Virulence of Campylobacter jejuni 81-176. Infection and Immunity, 68(8), 4384-4390.
Kim, E., Koo, T., Park, S. W., Kim, D., Kim, K., Cho, H., . . . Kim, J. (2017). In vivo genome editing with a small Cas9 orthologue derived from Campylobacter jejuni. Nature Communications, 8, 14500.
Shulman, S. T., Friedmann, H. C., & Sims, R. H. (2007). Theodor Escherich: The First Pediatric Infectious Diseases Physician? Clinical Infectious Diseases, 45(8), 1025-1029.
Parkhill, J., Wren, B. W., Mungall, K., Ketley, J. M., Churcher, C., Basham, D., . . . Barrell, B. G. (2000). The genome sequence of the food-borne pathogen Campylobacter jejuni reveals hypervariable sequences. Nature, 403(6770), 665-668.
C. jejuni falls under the Campylobacteraceae family, and the Campylobacter genus. Campylobacter jejuni was discovered by Theodor Escherich. In 1886, Escherich was studying stool specimens and large intestinal mucous correlated to diarrhea in kittens and in neonates. He published his result in “The Intestinal Bacteria of the Infant and Their Relation to the Physiology of Digestion”. Escherich would grow cultures from infant stool samples and he successfully identified 19 different bacteria including Campylobacter jejuni.
C. jejuni is one of the highest causes of food poisoning in the United States. In 2011, the CDC predicted over 845,000 C. jejuni-related illness each year.
One particular strain of C. jejuni, strain NCTC11168, has a circular chromosome of only 1.6 million bp and two additional plasmids of 35 thousand bp each. Due to how small the C. jejuni genome is, it was genetically modified into CjCas9 for more efficient CRISPR-Cas9. Up to 1,654 proteins are predicted to be encoded by the C. jejuni genome.
Something very interesting about the C. jejuni genome is how few repeated sequences it has with only four repeated sequences consisting of three copies of the ribosomal RNA operon which are 6 thousand bp in size and three duplicates of the open reading frame. Repeated sequences are important as they could suggest highly preserved sequence, for example, the ribosomal RNA operon seen here. Repeated sequences are also important as tandem aid in mutations. A lack of repeated sequence suggests either slow mutation, or mutation through a different method.
Which brings us to another interesting fact about C. jejuni, its inability to perform DNA repair. C. jejuni does mutate, in fact some genomic regions show as much as three times more variation when compared with another organism like E. coli under similar conditions. This rapid phase of variation suggest that C. jejuni was unable to repair it’s own DNA. DNA sequencing found that the direct repair genes ada and phr, among other repair genes, were no where to be found in the C. jejuni sequence. C. jejuni mutates, simply by not repairing their DNA!!!
Another interesting fact about the C. jejuni genome is how few operons or cluster of genes there are. Some sets of proteins are still encoded by the same operons, for example the ribosomal protein operons. However, up to 617 families of genes are scatter through out the genome. For example, the Tyrosine, Aspartic Acid, and Glutamine synthesis genes can be found scattered randomly. While it seems to make it difficult to study, on the contrary, it allows us to focus on how important the genes that are grouped together must be. For example, the lipopolysaccharide gene clusters must have be involved in the synthesis of surface structures.
Isn’t C. jejuni interesting. Thank you for listening.
Bacon, D. J., Alm, R. A., Burr, D. H., Hu, L., Kopecko, D. J., Ewing, C. P., . . . Guerry, P. (2000). Involvement of a Plasmid in Virulence of Campylobacter jejuni 81-176. Infection and Immunity, 68(8), 4384-4390.
Kim, E., Koo, T., Park, S. W., Kim, D., Kim, K., Cho, H., . . . Kim, J. (2017). In vivo genome editing with a small Cas9 orthologue derived from Campylobacter jejuni. Nature Communications, 8, 14500.
Shulman, S. T., Friedmann, H. C., & Sims, R. H. (2007). Theodor Escherich: The First Pediatric Infectious Diseases Physician? Clinical Infectious Diseases, 45(8), 1025-1029.
Parkhill, J., Wren, B. W., Mungall, K., Ketley, J. M., Churcher, C., Basham, D., . . . Barrell, B. G. (2000). The genome sequence of the food-borne pathogen Campylobacter jejuni reveals hypervariable sequences. Nature, 403(6770), 665-668.