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Chapter 27 : Comparative Genomics of Stress Response Systems in Bacteria

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Abstract:

This chapter describes the approaches and results of comparative genomic analysis of with an emphasis on stress response systems and their impact on contemporary models of extreme ionizing radiation (IR) resistance. Clusters of orthologous genes (COGs) are the most useful framework for comparative genomics. Researchers assigned the proteins of to tdCOGs, which has reinforced the view of the proliferation of genes involved in stress response pathways. Gene expression in recovering from high-dose irradiation has been investigated using whole genome microarrays, which identified hundreds of genes that were upregulated during recovery. The radiation/desiccation response (RDR) regulon is dominated by DNA repair genes, including the recombinational repair proteins RecA and RecQ, the mismatch repair proteins MutS and MutL, and the UvrB and UvrC proteins, which are involved in nucleotide excision repair. The prospect of comparative genomics helping researchers resolve the seemingly paradoxical mechanism of extreme IR resistance in is good. Based on historical and contemporary research, it now seems evident that the extreme IR resistance phenotype of stems from a subtle regulatory interplay between diverse but widespread systems including Mn homeostasis, metabolite regulation, respiratory control, macromolecular degradation, and other oxidative stress response pathways.

Citation: Makarova K, Daly M. 2011. Comparative Genomics of Stress Response Systems in Bacteria, p 445-457. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch27

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Nucleotide Excision Repair
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Transmission Electron Microscopy
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Reactive Oxygen Species
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Figure 1.

Model of ionizing radiation-driven manganese and iron redox cycling. Water is the most abundant chemical found in living cells and the primary ROS known to arise during the radiolysis of HO are hydroxyl radicals (HO → HO+ H [proton] + e [hydrated electron]) (Daly, ; von Sonntag, ); hydrogen peroxide (2 HO HO) (Daly, ; von Sonntag, ); and superoxide anions (O + e O ) (Daly, ; von Sonntag, ). Immediate cellular damage during exposure to IR is typically attributed to HO. Whereas HO radicals are extremely reactive and short-lived, O and HO are relatively inert and long-lived (Daly, ; von Sonntag, ); this, however, does not imply that HO will display greater toxicity. For ROS, high reactivity without specificity is distributed uniformly across cell targets; low reactivity with high specificity is focused on particular cellular targets (Omar et al., ). A secondary source of HO in cells during irradiation is the Fenton reaction, which is one of the most powerful oxidizing reactions known and involves the catalytic decomposition of HO by ferrous ions (HO + Fe(II) Fe(III) + OH+ HO); the analogous reaction with Mn(II) does not occur (Daly et al., ). The most consequential damage by O and HO in cells is to proteins which contain exposed iron-sulfur or haem groups (Imlay, ), to proteins which contain cysteine residues (Omar et al., ; Yan, ), and to proteins containing cationbinding sites where an iron-catalyzed site-specific oxidation occurs (Stadtman and Levine, ). It follows that the survival of irradiated enzymes and their hosts rests on preventing both nonspecific (HO) and site-specific (O and HO) forms of ROS damage. Under IR, Fe(II, III) redox cycling is predicted to generate HO and O , whereas Mn(II, III) redox cycling is predicted to favor O scavenging without HO production. Thus, manganese complexes are predicted to prevent the proliferation of iron-dependent ROS and protect diverse cellular functions (Daly, ; Daly et al., ; Daly et al., ).

Citation: Makarova K, Daly M. 2011. Comparative Genomics of Stress Response Systems in Bacteria, p 445-457. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch27
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Tables

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Table 1.

Protein family expansions specific for the lineage

Citation: Makarova K, Daly M. 2011. Comparative Genomics of Stress Response Systems in Bacteria, p 445-457. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch27
Generic image for table
Table 2.

Protein family expansions specific for the lineage

Citation: Makarova K, Daly M. 2011. Comparative Genomics of Stress Response Systems in Bacteria, p 445-457. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch27
Generic image for table
Table 3.

Selected D. radiodurans genesimplicatedinradiationresistance

Citation: Makarova K, Daly M. 2011. Comparative Genomics of Stress Response Systems in Bacteria, p 445-457. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch27

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