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Chapter 18 : Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition

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Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition, Page 1 of 2

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Abstract:

The study of the phenomenon of contact-dependent growth inhibition (CDI) began with the observation that in mixed cultures of , an strain from the intestine of a rat designated EC93 inhibited the growth of differentially marked (antibiotic resistances) K-12 bacteria in the same culture. The authors say that they are not aware of the function(s) of contact-dependent growth inhibition (CDI) systems in the many different bacterial genera containing CDI homologues at the time of the writing this chapter, although progress in this area is being made. The chapter is an account of the genetic approaches the authors have used to explore CDI, including some anomalies and stumbling blocks that may be of interest to the reader. To identify the cellular factors that play roles in CDI, the authors took a series of genetic approaches. Initially, a transposon EZ-Tn5<KAN-2> library was constructed in EPI100 ( Epicentre) target cells. To identify the cellular factors that play roles in CDI, the authors took a series of genetic approaches. They observed a number of mucoid colonies in selection scheme described from which insertions conferring CDI resistance were identified, as well as a similar mutant selection using chemical mutagenesis. To study the mechanism of contact-dependent growth inhibition, the authors developed a CDI autoinhibition system in which growth inhibition is regulated by controlling expression of the immunity gene. The necessity of an energy source for growth recovery raised the question of what role metabolism plays in CDI.

Citation: Aoki S, Low D. 2011. Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition, p 173-183. In Maloy S, Hughes K, Casadesús J (ed), The Lure of Bacterial Genetics. ASM Press, Washington, DC. doi: 10.1128/9781555816810.ch18

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Outer Membrane Proteins
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Bacterial Pathogenesis
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BAM Complex Proteins
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Figures

Image of FIGURE 1
FIGURE 1

Deletion mapping of the CDI region of EC93. Bars indicate the area of deleted cosmid insert. Deletions that maintain a CDI phenotype are indicated with solid lines. Deletions that have a CDI phenotype are indicated with dotted lines. The pDAL660Δ1–39 deletion clone referred to in the text is boxed.

Citation: Aoki S, Low D. 2011. Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition, p 173-183. In Maloy S, Hughes K, Casadesús J (ed), The Lure of Bacterial Genetics. ASM Press, Washington, DC. doi: 10.1128/9781555816810.ch18
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Image of FIGURE 2
FIGURE 2

Genetic approaches to identify the CDI pathway (see text).

Citation: Aoki S, Low D. 2011. Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition, p 173-183. In Maloy S, Hughes K, Casadesús J (ed), The Lure of Bacterial Genetics. ASM Press, Washington, DC. doi: 10.1128/9781555816810.ch18
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Image of FIGURE 3
FIGURE 3

Role of Kps K-15 capsule in CDI resistance. (A) EPI100 targets containing UPEC 536 cosmids pDAL747, pDAL748, or pDAL749 were screened for resistance to contact-dependent growth inhibition. Targets were mixed with CDI inhibitory at a 10:1 inhibitor to target cell ratio. Viable target cell counts were determined after 3 h. (B) Maps of the K-15 capsule-encoding gene cluster contained within the UPEC 536 genomic DNA insert of cosmids. The dotted line indicates the 15.6-kb section deleted from pDAL748Akps), (C) K-12 pDAL660A1-39 (CDI) inhibitors were competed against EPI100 targets containing pDAL748, pDAL748 with the capsule region deleted (pDAL748D or a vector control. Viable target cell counts at 0 and 3 h are depicted by closed and open bars, respectively.

Citation: Aoki S, Low D. 2011. Using Genetic Approaches To Delineate the Pathway of Contact-Dependent Growth Inhibition, p 173-183. In Maloy S, Hughes K, Casadesús J (ed), The Lure of Bacterial Genetics. ASM Press, Washington, DC. doi: 10.1128/9781555816810.ch18
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References

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