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Chapter 15 : The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis

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The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis, Page 1 of 2

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Abstract:

To persist in the environment, that is confronted with feeding amoebae, must avoid digestion and instead establish a protected site for intracellular replication. After exhausting the resources of its host, the bacterial progeny must vacate the premises to search out a more fertile locale. When encounters grazing amoebae, its prowess as a parasite becomes paramount. A model for the life cycle in which growth phase determines virulence expression and replication vacuole biogenesis has been provided in this chapter. A striking observation made by Brenda Byrne motivated the authors' investigation of virulence regulation. When broth cultures of exit the exponential growth (E) phase, the bacteria become osmotically resistant, sodium sensitive, cytotoxic, motile, infectious, and competent to evade macrophage lysosomes. Results obtained by four independent experimental approaches strengthen the hypothesis that survives and replicates within lysosomal compartments. First, virtually every vacuole that harbors more than five bacteria also contains LAMP-1. Second, bacteria within endosomal vacuoles are viable, as judged by their capacity to respond to a metabolic inducer by expressing a reporter gene. Third, replicating bacteria obtained from macrophages, but not broth, are acid resistant. Finally, inhibition of vacuole acidification and maturation by bafilomycin A1 or other agents actually inhibits bacterial replication.

Citation: Swanson M, Bachman M. 2002. The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis, p 74-81. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch15

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Image of FIGURE 1
FIGURE 1

A model for the life cycle in which growth phase determines virulence expression and replication vacuole biogenesis. In the PE phase, produces Dot-dependent (triangles) and -independent (coating) factors that immediately isolate its phagosome from the endosomal pathway (depicted as shaded vacuoles). During the next ∼8 h, the bacterium remains in lag phase, induces acid resistance, and down-regulates expression of virulence factors, including those that block fusion with the endosomal pathway. Next, autophagy, an endoplasmic reticulum (ER)-dependent process, delivers the phagosome to the lysosomal compartment, where replication continues. When nutrients become limiting, a stringent response-like mechanism induces virulence traits, including cytotoxicity, flagella, and factors that block phagosome maturation. Consequently, the bacterial progeny escape the spent host and seek a new replication site, where the cycle repeats. See text for details; times are approximate.

Citation: Swanson M, Bachman M. 2002. The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis, p 74-81. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch15
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Image of FIGURE 2
FIGURE 2

A stringent response model for virulence expression as a response to nutrient deprivation. When their amino acid supply is limited, bacteria accumulate uncharged tRNAs, which activate the ribosome-associated enzyme RelA. RelA converts GTP to the alarmone (p)ppGpp, a second messenger that positively activates the stationary phase sigma factor RpoS and an RpoS-independent regulatory factor (X). As a result, the bacteria exit the exponential growth phase and express a panel of traits that may promote bacterial survival and transmission in the environment. See the text for details.

Citation: Swanson M, Bachman M. 2002. The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis, p 74-81. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch15
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Image of FIGURE 3
FIGURE 3

Summary of the fate of virulent and avirulent within macrophages. In the postexponential (PE) phase, expresses Dot/lcm-dependent factors (triangles) to isolate the phagosome from the endosomal pathway. PE-phase bacteria must also produce a Dot/Icm-independent factor (coating) to block fusion with the terminal lysosomes, since that lacks Dot/Icm function or has been killed by formalin colocalizes with the late endosomal protein LAMP-1 but not with other markers of the lysosomes. In contrast, exponential (E)-phase traffic to lysosomes with the rapid kinetics observed for and heat-killed PE Early endosomes contain transferrin receptor (R), late endosomes contain LAMP-1, and lysosomes contain LAMP-1, cathepsin D, and accumulate endocytosed probes.

Citation: Swanson M, Bachman M. 2002. The Life Cycle: Connections between Growth Phase, Virulence Expression, and Replication Vacuole Biogenesis, p 74-81. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch15
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