Untitledon October 31, 2012
The role of 'soaking' in spiteful toxin production in
R. Fredrik Inglis, Alex R. Hall and Angus Buckling published online 29 August 2012 Biol. Lett. This article cites 18 articles, 7 of which can be accessed free
Article cited in:
Published online 29 August 2012 in advance of the print journal.
Articles on similar topics can be found in the following collections Email alerting service
Receive free email alerts when new articles cite this article - sign up in the box at the top right-hand corner of the article or click Advance online articles have been peer reviewed and accepted for publication but have not yet appeared in the paper journal (edited, typeset versions may be posted when available prior to final publication). Advance online articles are citable and establish publication priority; they are indexed by PubMed from initial publication.
Citations to Advance online articles must include the digital object identifier (DOIs) and date of initial Biol. Lett.
on October 31, 2012 R. F. Inglis et al.
large, smooth, green colonies, whereas O:9 forms small, wrinkly, white colonies. At the more extreme frequencies, antibiotic plates wererequired to give better resolution of colony counts, and this was possible due to the different antibiotic resistance profiles of the strains(O:9 is resistant to rifampicin 312.5 mg ml 1, PW5036 is resistant to tetracycline 312.5 mg ml 1, and PAO1 is resistant to rifampicin60 mg ml 1 and tetracycline 6 mg ml 1). Selection coefficients (S) were used to estimate at what frequency bacteriocin production is favoured in PW5036 relative to the wild type PAO1 using the common competitor O:9, where S ¼ (mPAO1/PW5036 mO:9)/mO:9,and (m) refers to ln(final density/starting density) . As no cells of the bacteriocin sensitive common competitor O:9 could bedetected at when present at frequencies of 1 and 10 per cent, we used the minimum detection level (200 cells ml 1) to calculate ourselection coefficients for these frequencies.
To control for intrinsic growth rate differences between PW5036 and the wild type PAO1, they were also competed against each other directly at a 1 : 1 ratio for 96 h and subsequently plated on KB agar and KB agar containing tetracycline to distinguish between both starting frequency of bacteriocin producers strains. Selection coefficients were calculated and PAO1 displayedan overall 2.7 per cent fitness advantage when compared with Figure 1. Difference in growth between the wild type strain PW5036 (results not shown). When calculating final selection coef (PAO1) with the ability to absorb and neutralize its own bacter ficients, this growth rate advantage of PAO1 was used to scale thegrowth of PW5036 (by multiplying its growth, represented by the iocins (i.e. ‘self soaking') and an isogenic strain lacking the FpvA term m in the equation for calculating selection coefficients, by receptor (PW5036) required for the absorption of the bacterio 2.7%) to allow for direct comparison between the two strains, cin when competing against a sensitive strain (O:9). The thereby taking into account only the difference in FpvA production.
receptor deficient strain shows an increased competitive advan However, even after taking into account this growth rate difference, tage over the wild type at higher and lower frequencies. Error we acknowledge that, though unlikely, other, unknown effects of bars show +1 s.e. of the mean. Filled circles, PW5036 losing the FpvA receptor may affect our results. All statistical analyses were performed in R (v. 2.9.2).
(non soaker) versus O:9; open circles, PAO1 (soaker) versus O:9.
5.16, p , 0.027). Pairwise comparisons between In our experiment, we compared the frequency- the two strains reveal greater fitness of the non-soaker at dependent fitness of a wild-type bacteriocin producer starting frequencies of 0.1 per cent (p , 0.0001), 1 per (PAO1) strain when competed with a bacteriocin- cent (p , 0.003), 10 per cent (p , 0.01), 90 per cent sensitive strain (P. aeruginosa serotype O:9), with that (p , 0.0001) and 99 per cent (p , 0.002) but no of a bacteriocin-producing ‘non-soaker' (PW5036, difference at 50 per cent (p . 0.62) after sequential deficient in its bacteriocin, S2, receptor, FpvA, but Bonferroni correction for multiple tests [ otherwise isogenic to wild-type PAO1) when competedwith the same bacteriocin-sensitive strain (O:9) ].
We confirmed that growth inhibition of the susceptible strain did not differ in the supernatant of wild-type and The costs of soaking are clearly most pronounced at both high and low frequencies. At high frequencies, was unaffected by the length of time strains were cul- this is entirely as expected because more wild-type tured before supernatant was extracted (F1,24 cells will inevitably lead to more soaking. The low- frequency effect, however, is initially more surprising, 0.23, p . 0.64). This result was also confirmed as less soaking inevitably occurs with fewer bacterio- when performing soft agar overlays containing the cinogenic cells. However, theory suggests that the fitness sensitive strain on both bacteriocin-producing strains reduction of competitors per bacteriocinogenic cell is (see the electronic supplementary material, figure S1) critically important in determining the frequency at ]. This strongly suggests that bacteriocin production which a bacteriocinogenic lineage can invade a susceptible did not differ between the wild-type and non-soaker population, or is driven to extinction: the greater the strains, hence differences in frequency-dependent fit- reduction in competitor fitness, the lower the frequency ness between the wild-type and non-soaker strain are at which bacteriocinogenic cells can invade ]. This presumably the result of soaking effects.
means that a reduction in competitor killing through soak- Selection coefficients were used to estimate the ing will have disproportionately greater effects at reducing fitness of the bacteriocin-producing wild-type, non- fitness at lower frequencies of the bacteriocinogenic line- soaker and sensitive strains ]. Both the wild-type age. At intermediate frequencies, costs of self-soaking and non-soaking strain show a unimodal relationship are likely to be minimal, because bacteriocins are between fitness and starting frequency, as previously produced in sufficient quantity to generate a large fitness described [, with both the wild-type (linear F1,31 advantage over susceptible bacteria.
20.76, p , 0.001; quadratic F1,30 29.64, p , 0.001) As well as investigating the effect of soaking on and non-soaking strain ), peaking at intermedi- frequency-dependent fitness, we were interested if soak- ate values (linear F1,31 10.7, p , 0.003; quadratic ing could contribute to the observed ability of sensitive 8.98, p , 0.005). However, when compared cells to persist when at initially low starting frequencies with the wild-type, the non-soaker peaks at higher [Whereas approximately 105 cells ml 1 survived starting frequencies and reaches overall higher levels competition with the wild-type (when the sensitive of selection coefficients (intercept: F1,61 strain (O:9) is at starting frequencies of 1 and 10%), 0.0001; strain by frequency by frequency interaction: none of the sensitive competitor strain (O:9) was on October 31, 2012 R. F. Inglis et al.
4 Brown, S. P., Le Chat, L., De Paepe, M. & Taddei, F.
strain at these frequencies (with a detection threshold 2006 Ecology of microbial invasions: amplification allows of approx. 200 cells ml 1). Note that the resulting virus carriers to invade more rapidly when rare. Curr.
selection coefficients for these two treatments are a Biol. 16, 2048 2052. (doi:10.1016/j.cub.2006.08.089) 5 Vigneux, F., Bashey, F., Sicard, M. & Lively, C. M. 2008 minimum and assume 200 cells ml 1 of the competitor.
Low migration decreases interference competition among Soaking may, therefore, contribute to the maintenance of parasites and increases virulence. J. Evol. Biol. 21, sensitive cells in both clinical and natural populations, 1245 1251. (doi:10.1111/j.1420 9101.2008.01576.x) and may contribute to the intransitive dynamics of 6 Inglis, R. F., Gardner, A., Cornelis, P. & Buckling, A.
producing, resistant and sensitive cells 2009 Spite and virulence in the bacterium Pseudomonas Under conditions where the producing strain is aeruginosa. Proc. Natl Acad. Sci. USA 106, 5703 5707.
dominant in the population, one would also expect the loss of the bacteriocin receptor, as strains without 7 Hawlena, H., Bashey, F. & Lively, C. M. 2010 The it would be able to outcompete the wild-type as they evolution of spite: population structure and bacteriocin no longer pay the costs of producing and expressing mediated antagonism in two natural populations of this receptor and are more effective at killing competi- Xenorhabdus bacteria. Evol. Int. J. Org. Evol. 64,3198 3204. (doi:10.1111/j.1558 5646.2010.01070.x) tors. However, in this system, FpvA is also responsible 8 Hamilton, W. D. 1963 The evolution of altruistic behav for the uptake of pyoverdine type I , an important iour. Am. Nat. 97, 354 356. (doi:10.1086/497114) iron-scavenging molecule, so its loss would be unlikely 9 Hamilton, W. D. 1970 Selfish and spiteful behaviour in to occur in iron-limited environments.
Soaking is likely to be important in the evolution of microbial toxin production in general. Many toxins 10 Hamilton, W. D. 1996 Innate social aptitudes of man: an target receptors that have important fitness conse- approach from evolutionary genetics. In Narrow roads of quences for competitors, which may often be shared gene land, pp. 327 351. Oxford, UK: W. H. Freeman.
by toxin-producing lineage. As such, selection to 11 Riley, M. A. & Wertz, J. E. 2002 Bacteriocins: evolution, target common bacterial receptors may be constrained ecology, and application. Annu. Rev. Microbiol. 56, 117137. (doi:10.1146 by the need to produce increased quantities of bacter- 12 Chao, L. & Levin, B. R. 1981 Structured habitats and the iocins. Moreover, this soaking effect also suggests evolution of anticompetitor toxins in bacteria. Proc. Natl another important role of community context in driv- Acad. Sci. USA 78, 6324 6328. (doi:10.1073/pnas.78.
ing evolutionary dynamics. The extent to which bacteriocins can bind to receptors for other species is 13 Michel Briand, Y. & Baysse, C. 2002 The pyocins of unclear, but cases have been identified where interspe- Pseudomonas aeruginosa. Biochimie 84, 499 510. (doi:10.
cies inhibitions occur Finally, the increase in 1016/S0300 9084(02)01422 0) the short-term efficacy of receptor-less mutants, as 14 Jacobs, M. A. et al. 2003 Comprehensive transposon well as their inevitable long-term cost through their mutant library of Pseudomonas aeruginosa. Proc. Natl inability to use siderophores, suggests a potential role Acad. Sci. USA 100, 14 339 14 344. (doi:10.1073/ in the biocontrol of clinical and agricultural infections.
15 Denayer, S., Matthijs, S. & Cornelis, P. 2007 Pyocin S2 ¨ mmerli and four anonymous reviewers for (Sa) kills Pseudomonas aeruginosa strains via the FpvA their very useful comments and suggestions. This work was funded by the European Research Council, the Leverhulme 7663 7668. (doi:10.1128/JB.00992 07) Trust and the Natural Environment Research Council.
16 Fyfe, J. A. M., Harris, G. & Govan, J. R. W. 1984 Revised pyocin typing method for Pseudomonas aeruginosa. J. Clin.
Microbiol. 20, 47 50.
17 Lenski, R. E., Rose, M. R., Simpson, S. C. & Tadler, 1 West, S. A., Diggle, S. P., Buckling, A., Gardner, A. & Griffins, A. S. 2007 The social lives of microbes. Annu.
Escherichia coli. I. Adaptation and divergence during Rev. Ecol. Evol. Syst. 38, 53 77. (doi:10.1146/annurev.
2000 generations. Am. Nat. 138, 1315 1341. (doi:10.
2 Gardner, A., West, S. A. & Buckling, A. 2004 Bacterio 18 Holm, S. 1979 A simple sequentially rejective multiple cins, spite and virulence. Proc. R. Soc. Lond. B 271, test procedure. Scand. J. Stat. 6, 65 70. (doi:10.2307/ 1529 1535. (doi:10.1098/rspb.2004.2756) 3 Massey, R. C., Buckling, A. & Ffrench Constant, R.
19 Kerr, B., Riley, M. A., Feldman, M. W. & Bohannan, 2004 Interference competition and parasite virulence.
B. J. M. 2002 Local dispersal promotes biodiversity in a Proc. R. Soc. Lond. B 271, 785 788. (doi:10.1098/ rock paper scissors.
171 174. (doi:10.1038/nature00823)
ATHLETICS OMNIBUS - ILLEGAL SUBSTANCES IN SPORT From the Boland Athletics website: www.bolandathletics.com THE USE OF PROHIBITED SUBSTANCES IN SPORT A PROHIBITED CLASSES OF SUBSTANCES The International Association of Athletics Federations (IAAF) rule 144 states clearly that any method used to enhance performance artificially is illegal.
拒绝荷尔蒙失调 英文版 欣赏
What are hormones？Hormones are chemical messengers that flow through our bloodstream and enter tissues where they turn on switches to the genetic machinery, affecting the action of every cel in our body, either helping or ruining our lives depending on their balance, quantity, strength and body's reaction! Hormones are made in the ovaries, testes, adrenals, pituitary, pancreas, brain, thyroid, parathyroid and hypothalamus, just to name a few. These organs are also known as glands and belong to the bigger and more complex system: the endocrine system, which is like a symphony with several glands working both alone and together to orchestrate bodily functions. To put it in an analogy, "Touch one strand and the whole web trembles."