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Chapter 27 : The Genome

Authors: Richard A. Alm1, Brian Noonan1
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Affiliations: 1: Infection Discovery, AstraZeneca R&D Boston, 35 Gatehouse Drive, Waltham, MA 02451
Content Type: Monograph
Publication Year: 2001

Category: Bacterial Pathogenesis

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The Genome, Page 1 of 2

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Abstract:

A milestone in microbial genomics was set when became the first bacterial species to have its genome sequenced and compared from two independent isolates. Studies that sampled the entire genome and addressed nucleotide differences, such as randomly amplified polymorphic DNA (RAPD)-polymerase chain reaction (PCR), also provided a picture of extensive nucleotide diversity and showed that any particular strain could be distinguished from essentially all other strains. Other techniques such as PCR restriction fragment length polymorphism (RFLP), oligofingerprinting, restriction fragment end labeling, and ribotyping supported these observations. As with most microbial genome sequencing projects to date, J99 and 26695 were sequenced using a random shotgun approach from libraries of cloned chromosomal fragments of ~2.5 kb. The transcription and translation processes in appear to bear a lot of similarities to those of other gram-negative bacteria. Bacterial factors such as strain-specific genes (either chromosomally encoded or present on plasmids), differential gene expression (potentially mediated by methylation and pseudogene generation), phase variation (mediated by slippedstrand repair), or allelic variation (such as found in cagA, which plays a role in the level of phosphorylation of the CagA protein) may play a critical role in disease development. The application of techniques such as expression profiling with both human and bacterial microarrays should help answer many of the questions relating to the unique host-pathogen interaction.

Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
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The Genome
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Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
/content/10.1128/9781555818005.chap27.fig27-1
Figure 1

Comparison of the chromosomal organization of the two sequenced H. pylori genomes. The continuous outer circle represents the H. pylori 26695 genome whereas the inner circle represents the organization of the H. pylori J99 genome relative to that of strain 26695, incorporating artificial breaks to facilitate the alignment as described in the text and elsewhere ( ). The artificial breaks are represented by encircled numbers and represent inversions and/or translocations. The locations of complete (circle) or partial (half-circle) IS605 (filled) and IS606 (open) insertion elements in both chromosomes are indicated, and the five cases of coincident location are indicated by an asterisk (*) between the circles. The location and number of strain-specific genes (found in one strain but not the other) are indicated by vertical marks crossing the respective chromosome. At loci where both genomes possess strain-specific genes at the same position, the vertical mark crosses both genomic circles. The strain-specific genes boxed represent HP1383 and HP1404, which are found at either endpoint of genomic rearrangement 8. In this figure, the mpA and mpB genes of the IS605 and IS606 elements (a total of 2 in J99 and 14 in 26695) are included with the strain-specific genes. The location of the one and two plasticity zone(s) in J99 and 26695, respectively, are represented by stars (*).

10.1128/9781555818005/fig27-1_thmb.gif
10.1128/9781555818005/fig27-1.gif
Image of Figure 1
Figure 1

Comparison of the chromosomal organization of the two sequenced H. pylori genomes. The continuous outer circle represents the H. pylori 26695 genome whereas the inner circle represents the organization of the H. pylori J99 genome relative to that of strain 26695, incorporating artificial breaks to facilitate the alignment as described in the text and elsewhere ( ). The artificial breaks are represented by encircled numbers and represent inversions and/or translocations. The locations of complete (circle) or partial (half-circle) IS605 (filled) and IS606 (open) insertion elements in both chromosomes are indicated, and the five cases of coincident location are indicated by an asterisk (*) between the circles. The location and number of strain-specific genes (found in one strain but not the other) are indicated by vertical marks crossing the respective chromosome. At loci where both genomes possess strain-specific genes at the same position, the vertical mark crosses both genomic circles. The strain-specific genes boxed represent HP1383 and HP1404, which are found at either endpoint of genomic rearrangement 8. In this figure, the mpA and mpB genes of the IS605 and IS606 elements (a total of 2 in J99 and 14 in 26695) are included with the strain-specific genes. The location of the one and two plasticity zone(s) in J99 and 26695, respectively, are represented by stars (*).

Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
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Figure 2

Genomic location of the conserved orthologous genes between H. pylori J99 and 26695. The nucleotide position of the initiation codon of each orthologous gene-pair (♦) in J99 and 26695 was plotted. The disruption of the conserved gene order of the orthologs is easily detected. The genes affected by the artificial breaks introduced to align the orthologous genes from the two genomes are encircled and numbered according to the inversion and/or translocation number given in Fig. 1 . Due to the resolution, the smallest inversion (number 5) cannot be detected, but its location is indicated with an arrow. The locations of the plasticity zones (PZ) are indicated. Due to their large size, the location of the coincident plasticity zone is represented by a gap in the diagonal “orthologous gene line. ” The other plasticity zone (split by rearrangement 3) in 26695 is located at approximately 0.45 Mb on the 26695 chromosome.

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10.1128/9781555818005/fig27-2.gif
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Figure 2

Genomic location of the conserved orthologous genes between H. pylori J99 and 26695. The nucleotide position of the initiation codon of each orthologous gene-pair (♦) in J99 and 26695 was plotted. The disruption of the conserved gene order of the orthologs is easily detected. The genes affected by the artificial breaks introduced to align the orthologous genes from the two genomes are encircled and numbered according to the inversion and/or translocation number given in Fig. 1 . Due to the resolution, the smallest inversion (number 5) cannot be detected, but its location is indicated with an arrow. The locations of the plasticity zones (PZ) are indicated. Due to their large size, the location of the coincident plasticity zone is represented by a gap in the diagonal “orthologous gene line. ” The other plasticity zone (split by rearrangement 3) in 26695 is located at approximately 0.45 Mb on the 26695 chromosome.

Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
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Tables

The Genome
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Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
/content/10.1128/9781555818005.chap27.tab27-1
Table 1

General comparative features of the

10.1128/9781555818005/tab27-1_thmb.gif
10.1128/9781555818005/tab27-1.gif
Generic image for table
Table 1

General comparative features of the

Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27
/content/10.1128/9781555818005.chap27.tab27-2
Table 2

Genes unique to either J99 or 26695

10.1128/9781555818005/tab27-2_thmb.gif
10.1128/9781555818005/tab27-2.gif
Generic image for table
Table 2

Genes unique to either J99 or 26695

Citation: Alm R, Noonan B. 2001. The Genome, p 295-311. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch27

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