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Journal of Bacteriology, October 1998, p. 5398-5405, Vol. 180, No. 20
Section of Microbiology, Cornell University, Ithaca, New
York 14853,1
Department of Biology,
Trinity University, San Antonio, Texas
78212,2 and
Department of Chemistry,
Ithaca College, Ithaca, New York
148503
Received 23 March 1998/Accepted 28 July 1998
The TraR and TraI proteins of Agrobacterium tumefaciens
mediate cell-density-dependent expression of the Ti plasmid
tra regulon. TraI synthesizes the autoinducer pheromone
N-(3-oxooctanoyl)-L-homoserine lactone
(3-oxo-C8-HSL), while TraR is an
3-oxo-C8-HSL-responsive transcriptional activator. We have
compared the abilities of 3-oxo-C8-HSL and 32 related
compounds to activate expression of a TraR-regulated promoter. In a
strain that expresses wild-type levels of TraR, only
3-oxo-C8-HSL was strongly stimulatory, four compounds were detectably active only at high concentrations, and the remaining 28 compounds were inactive. Furthermore, many of these compounds were
potent antagonists. In contrast, almost all of these compounds were
stimulatory in a congenic strain that overexpresses TraR and no
compound was a potent antagonist. We propose a model in which
autoinducers enhance the affinity of TraR either for other TraR
monomers or for DNA binding sites and that overexpression of TraR
potentiates this interaction by mass action. Wild-type A. tumefaciens released a rather broad spectrum of autoinducers, including several that antagonize induction of a wild-type strain. However, under all conditions tested, 3-oxo-C8-HSL was more
abundant than any other analog, indicating that other released
autoinducers do not interfere with tra gene induction. We
conclude that (i) in wild-type strains, only 3-oxo-C8-HSL
significantly stimulates tra gene expression, while many
autoinducer analogs are potent antagonists; (ii) TraR overexpression
increases agonistic activity of autoinducer analogs, allowing sensitive
biodetection of many autoinducers; and (iii) autoinducer stimulatory
activity is potentiated by TraR overproduction, suggesting that
autoinducers may shift an equilibrium between TraR
monomers and dimers or oligomers. When autoinducer
specificities of other quorum-sensing proteins are tested, care should
be taken not to overexpress those proteins.
Many genera of bacteria use
diffusible chemicals to exchange information (3, 5, 12, 18, 26,
36, 41, 45). An important class of chemical signal molecules is
the family of N-acyl-homoserine lactones
(N-acyl-HSLs), which are generally synthesized by an enzyme
related to the LuxI protein of Vibrio fischeri. These
compounds, called autoinducers, passively diffuse across the bacterial envelope and therefore accumulate intracellularly only at high bacterial densities (25). These chemicals are
thought to bind to a protein related to the LuxR protein of
V. fischeri, whose amino terminus contains an
autoinducer binding site and whose carboxyl terminus
binds to a DNA site directly upstream of the lux promoter
(1, 7, 21, 42). Cell density-dependent gene expression is
denoted quorum sensing, and this sort of regulation is used by a wide
spectrum of bacteria to regulate diverse genes, including the
pathogenicity genes of several plant and animal pathogens.
The Ti plasmids of several Agrobacterium tumefaciens strains
bear genes that encode a LuxI-type protein called TraI, which synthesizes N-(3-oxooctanoyl)-L-HSL
(3-oxo-C8-HSL) and a LuxR-type protein called TraR, which
presumably binds 3-oxo-C8-HSL (17, 23, 30, 34,
46). Putative TraR-autoinducer complexes activate transcription of several genes required for Ti plasmid conjugal transfer as well as other Ti plasmid-borne genes. As expected, Ti
plasmid conjugation occurs only at high donor population
densities (16). The expression of TraR is regulated by
particular opines (17). Octopine induces expression of the
traR genes of plasmids related to pTi15955, pTiA6, and
pTiR10, while agrocinopines A and B induce the traR gene of
pTiC58 (4, 17). These observations explain older findings
that Ti plasmid conjugation occurs only within crown gall tumors or in
the presence of particular opines (9). The traR
and traI genes are positively autoregulated (17).
All autoinducers described to date contain an HSL
moiety and a fatty acyl group whose members have various lengths,
saturation levels, and oxidation states. Two of these
compounds have been shown to derive their fatty acids from
acyl-ACP (22, 30, 38), which indicates that these fatty
acids are drawn from pools of fatty acid biosynthetic intermediates.
The fatty acids of acyl-ACPs always have even numbers of carbon
atoms. They also have either 3-oxo, 3-hydroxyl, or fully
reduced methylene groups at the C-3 position or a have a 2,3 unsaturated bond (8). Accordingly, the acyl groups of all
natural autoinducers have even numbers of carbon atoms
and have 3-oxo, 3-hydroxyl, or fully reduced acyl groups. Curiously, no
autoinducer has been reported to contain a 2,3 unsaturated bond in its acyl moiety, although two
autoinducers have 7,8 unsaturated bonds (20, 35,
39). The lengths of these side chains contain between 4 and 14 carbon atoms.
In several studies, the ability of autoinducer analogs
to induce expression of quorum-sensing systems has been tested (6, 13, 19, 32, 37, 46). In general, compounds closely related to the
cognate autoinducer caused weak-to-moderate gene
expression while less similar compounds were less active. In some
cases, autoinducer analogs acted as antagonists of the
native autoinducer and thereby inhibited the induction
of target genes. In two studies, autoinducer analogs
were demonstrated to inhibit binding of radiolabeled autoinducers (32, 37).
There are a few reports of a single LuxI-type protein synthesizing more
than one autoinducer. LuxI synthesizes primarily
3-oxo-C6-HSL (see Fig. 1, compound C) but also synthesizes
small amounts of C6-HSL (compound K; see reference 27).
Similarly, an Escherichia coli strain expressing the
LasI protein of Pseudomonas aeruginosa synthesizes primarily
3-oxo-C12-HSL but also synthesizes trace amounts of
additional compounds, including two that coelute by reversed-phase high-performance liquid chromatography (HPLC) with 3-oxo-C6-HSL and 3-oxo-C8-HSL (33,
44). The SwrI protein of Serratia liquefaciens
synthesizes both C4-HSL and C6-HSL in a 10:1
ratio (14). HPLC fractionation of Agrobacterium
autoinducers revealed two bioactive fractions
(46). One fraction contained 3-oxo-C8-HSL, while
a second, less homogeneous, fraction contained compounds having
molecular masses of 274, 214, and 200 Da. While the 274-Da compound was
thought to be due to a purification artifact, the other two compounds
were not since they had molecular masses identical to those of
3-oxo-C6-HSL and C6-HSL, respectively.
That study did not determine whether all three compounds were
synthesized by TraI.
Shaw and colleagues recently described an elegant method for using an
A. tumefaciens strain to detect a broad range of
autoinducers (40). The strain used in these
studies was able to recognize no fewer than nine
autoinducers having a wide variety of acyl side groups.
However, in an earlier report, an A. tumefaciens strain
discriminated between different autoinducers far more
strongly (46). One difference between these two studies is
the genotypes of the bioassay strains. In the present study, we
evaluated whether differences in the traR genotype that
affect its expression level might alter the ability of A. tumefaciens to detect analogs of 3-oxo-C8-HSL. We
report that TraR overproduction allows A. tumefaciens to detect a broad range of autoinducer analogs and
abolishes the ability of autoinducer analogs to act
as antagonists.
Strains and plasmids.
WCF47 is a derivative of R10
(10) containing a nonpolar internal deletion of
traI. The traI deletion was constructed with two
fragments generated by PCR, one containing the 5' end of
traI and upstream sequences and the other containing the 3'
end of traI and downstream sequences. These fragments were
ligated together, and the resulting traI deletion was
introduced into the suicide plasmid pKNG101 (24). The
resulting plasmid, pCF393, was introduced into strain R10 by
conjugation and selected with streptomycin. Streptomycin-resistant
transconjugants were plated on solid medium lacking streptomycin and
containing 5% sucrose. The sacB gene of pCF393 confers
sucrose sensitivity, and sucrose therefore selects for Campbell-type
excision. Sucrose-resistant derivatives were screened for the inability
to produce 3-oxo-C8-HSL. pCF218 is an IncP plasmid that
expresses TraR from a vector promoter (17), while pCF372
contains a PtraI-lacZ fusion (16).
Synthesis of autoinducer analogs.
The
chemical structures of autoinducer analogs used in this
study are shown in Fig. 1. Synthesis of
compounds A, E, I, J, K, L, M, and N was previously described
(13). Synthesis of compounds B, T, and Y was as described in
reference 37, while synthesis of compounds C and G was as described in
references 11 and 33, respectively.
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Analogs of the Autoinducer 3-Oxooctanoyl-Homoserine Lactone
Strongly Inhibit Activity of the TraR Protein of
Agrobacterium tumefaciens
ABSTRACT
Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
View larger version (20K):
[in a new window]
FIG. 1.
Chemical structures of N-acyl-HSL compounds
used in this study. Non-IUPAC descriptions of compounds are as follows:
A, 3-oxobutanoyl-HSL; B, 3-oxopentanoyl-HSL; C, 3-oxohexanoyl-HSL; D,
3-oxoheptanoyl-HSL; E, 3-oxooctanoyl-HSL; F, 3-oxoundecanoyl-HSL; G,
3-oxododecanoyl-HSL; H, 4-oxa-3-oxohexanoyl-HSL; I, butanoyl-HSL; J,
pentanoyl-HSL; K, hexanoyl-HSL; L, heptanoyl-HSL; M, octanoyl-HSL; N,
decanoyl-HSL; O, dodecanoyl-HSL; P, 3-hydroxynonanoyl-HSL; Q,
3-hydroxydodecanoyl-HSL; R, 2-butenoyl-HSL; S, 2-pentenoyl-HSL; T,
2-hexenoyl-HSL; U, 2-octenoyl-HSL; V, 2-nonenoyl-HSL; W,
2-decenoyl-HSL; X, 2-butynoyl-HSL; Y, 2-hexynoyl-HSL; Z,
5-hexynoyl-HSL; AA, 2-octynoyl-HSL; AB, 3-oxo-7-octynoyl-HSL; AC,
3-oxo-11-octadecenoyl-HSL; AD, diHSL-decandioate; AE,
diHSL-3,12-dioxotetradecandioate; AF, p-propylbenzoyl-HSL;
and AG, O-hexyl-N-HSL carbamate.
Bioassays of autoinducer activity.
Autoinducer analogs were stored in ethyl acetate at 
80°C. Prior to
use, autoinducers were warmed to room temperature and 0.017 µmol was added in 34 µl of ethyl acetate to empty culture tubes. After the solvent was allowed to evaporate, 1.75 ml of AT medium
(43) supplemented with 400 µg of octopine per ml and approximately 107 bacterial cells [strain
WCF47(pCF372) or WCF47(pCF372)(pCF218)] was added. After
the autoinducer analog was allowed to dissolve, 0.55 ml
was removed and added to 1.2 ml of the same culture (a 3.16-fold
dilution). This dilution was repeated serially nine times, resulting in
10 culture tubes having analogs at concentrations ranging from
10
1 to 104 to nM. These cultures were
incubated with aeration for 12 h and assayed for 
-galactosidase
specific activity (29). The bacterial cultures remained in
exponential growth phase during this interval. To assay the abilities
of analogs to prevent induction, the assays described above were
repeated, except that 3-oxo-C8-HSL (final concentration,
102 nM) was added in addition to the indicated amounts of
other compounds.
Western immunoblots of TraR. To compare intracellular concentrations of TraR in the two bioassay strains described above, we cultured each strain in 100 ml of AT broth containing 100 nM 3-oxo-C8-HSL to an optical density at 600 nm of 0.6, concentrated the cultures by centrifugation, resuspended the cultures in 1 ml of TEDG (50 mM Tris-HCL [pH 7.9], 0.5 mM EDTA, 1 mM dithiothreitol, 5% glycerol), disrupted the cells using a French pressure cell, and ultracentrifuged the lysates at 150,000 × g for 30 min. The resulting cleared lysates were size fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to a nitrocellulose membrane, and detected with affinity-purified polyclonal anti-TraR rabbit antiserum.
TLC analysis of autoinducers released by
A. tumefaciens.
The isolation of
autoinducers by strains expressing TraI was done by
culturing strains to stationary phase in 20 ml of broth, removing
bacteria by centrifugation, and extracting the cell-free spent broth
three times with 3 volumes of ethyl acetate. In control experiments,
this procedure was shown to recover virtually all of the
3-oxo-C8-HSL and 3-oxo-C6-HSL, although it may
not result in quantitative recovery of more polar compounds. The ethyl
acetate fractions were pooled and evaporated to dryness, and each
residue was resuspended in 1 ml of ethyl acetate, transferred to a 1-ml glass vial, and reevaporated. The residue was resuspended in 200 µl
of ethyl acetate and stored at 80°C. Aliquots (1 µl) were applied
to C18 reversed-phase thin-layer chromatography (TLC) plates (Whatman) and chromatographed with 60% methanol-40% water as
described previously (40). After chromatography, the
plates were dried and overlaid with 200 ml of agar containing AT
medium, 40 µg of X-Gal
(5-bromo-4-chloro-3-indolyl--D-galactopyranoside), and approximately 107 bacteria per ml [strain
WCF47(pCF372)(pCF218)]. TLC plates were incubated overnight at
28°C and examined for X-Gal hydrolysis.
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RESULTS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Recognition of autoinducer analogs by a strain
expressing wild-type levels of TraR.
We assayed 33 autoinducers and chemically related compounds (Fig. 1)
for the ability to induce -galactosidase activity in strain
WCF47(pCF372), which lacks its own traI gene and which has a plasmid-borne PtraI-lacZ fusion. Synthetic
3-oxo-C8-HSL (compound E) detectably activated this fusion
at a concentration of 3.0 nM (Fig. 2). A
concentration of 104 nM caused production of approximately
700 U of enzyme activity. The dose-response curve shown in Fig. 2
suggests that this regulatory system was not saturated by a
104 nM concentration of this autoinducer.
In marked contrast to these results, of the 32 other compounds tested,
only four caused production of significant levels of -galactosidase
activity (Fig. 2 and Table 1). These
compounds are 3-oxo-C7-HSL (compound D),
3-oxo-C11-HSL (F), 3-oxo-C12-HSL (G), and
3-oxo-7-octynoyl-HSL (AB). All of these compounds closely resemble
3-oxo-C8-HSL, differing only in the length or level of
desaturation of the acyl moeity. All compounds except
3-oxo-C8-HSL were weakly active or inactive at concentrations less than 103 nM (Fig. 2).
|
), D (
), F (
), G
(
), and AB (
) are shown. All other compounds were inactive.
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Autoinducer recognition by a strain that overexpresses
TraR.
To determine whether TraR overexpression altered the
detection of autoinducers, we constructed a derivative
of WCF47(pCF372) that contains plasmid pCF218, which bears
DNA that overexpresses TraR from a vector promoter (17).
While WCF47(pCF372) synthesizes extremely low levels of TraR,
WCF47(pCF372)(pCF218) synthesizes amounts that are
readily detectable by Western immunoblotting (Fig.
3). WCF47(pCF372)(pCF218) was far
more sensitive to low concentrations of 3-oxo-C8-HSL than
its parent, since it was detectably induced at concentrations as low as
0.1 nM and the response was saturated by an approximately 10 nM
concentration of this autoinducer (Fig.
4A). The reporter fusion in this strain,
when fully induced, expressed about twofold more -galactosidase than
the same reporter fusion in the strain that expresses wild-type levels
of TraR.
|
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), C (
), D (
); (B) results with compounds E (Production of multiple autoinducers by TraI. We have shown that several naturally occurring autoinducers are potent antagonists of 3-oxo-C8-HSL in a strain that expresses wild-type levels of TraR. In an earlier report, Zhang and colleagues reported that an A. tumefaciens strain containing an octopine-type Ti plasmid synthesized compounds having molecular masses identical to those of 3-oxo-C8-HSL, 3-oxo-C6-HSL, and C6-HSL (46). We have found that the latter two compounds can antagonize 3-oxo-C8-HSL. To determine whether A. tumefaciens synthesizes inhibitory concentrations of these compounds, we used TLC (40) to visualize all bioactive autoinducers made by A. tumefaciens and to estimate the concentrations of some of these compounds.
Strain R10(pCF372) was cultured in broth (AT salts supplemented with octopine) to stationary phase and assayed for-galactosidase activity. The culture expressed only 36 U of activity, indicating that
its tra regulon was only weakly induced and suggesting that the culture medium contained only limited amounts of
autoinducers. These data agree with earlier
observations that the high cell densities required for induction of
this system are more readily achieved on semisolid medium than in broth
culture (17). We therefore diluted this culture fivefold
into fresh broth (AT salts and octopine) and incubated it once
again to stationary phase. This second culture expressed 282 U of
-galactosidase activity, indicating that its tra regulon
was far more strongly induced than that of the first culture,
presumably due to the autoinducers released during the
first growth interval. Bacteria were removed by centrifugation from 20 ml of this culture, and the cell-free supernatant was extracted and
resuspended in 200 µl of ethyl acetate as described in Materials and
Methods. The concentrated extract was serially diluted in fivefold
steps, and 1 µl of each dilution was applied to a reversed-phase TLC
plate.
In the most concentrated sample, no fewer than six bioactive compounds
were detected (Fig. 5A). The two most
prominent spots had Rfs identical to those of
3-oxo-C8-HSL and 3-oxo-C6-HSL, and smaller
amounts of a compound with an Rf identical to
that of C6-HSL was also detected, consistent with the data
of Zhang and colleagues (46). In addition, trace amounts of
several more hydrophobic compounds were detected. Two very polar
compounds were also detected, as described more fully below.
WCF47(pCF372), which lacks traI, did not synthesize any
compounds active in this assay (data not shown), suggesting that all
detected compounds were synthesized by TraI.
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DISCUSSION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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We have tested the ability of two strains of A. tumefaciens to discriminate between the autoinducer 3-oxo-C8-HSL and a variety of related compounds. The strain expressing wild-type levels of TraR was far more strongly induced by its cognate autoinducer than by any other tested compound and was completely nonresponsive to all but four analogs. In contrast, an isogenic strain that constitutively overexpressed TraR was far more sensitive to these compounds and seemed to be less discriminatory, since 29 of the 33 compounds tested were stimulatory and several of these showed a half-maximal responses at only 3 to 30-fold-higher concentrations than that of the native autoinducer. Furthermore, in the strain expressing wild-type levels of TraR, many analogs were potent inhibitors of induction, while in a strain that overexpressed TraR, inhibition was not detected.
The narrow substrate specificities of wild-type strains might be interpreted to mean that only 3-oxo-C8-HSL and a few closely related compounds can bind TraR at the concentrations used. However, this possibility is inconsistent with our finding that many of the same compounds are potent antagonists, since this antagonism is presumably a consequence of competition for autoinducer binding sites. We therefore prefer a model in which TraR can bind a wide variety of autoinducer analogs but in which only a small subset can cause a conformational change in TraR necessary to convert it to an active form.
As described above, the strain expressing wild-type levels of TraR was stimulated only by compounds that closely resemble the cognate autoinducer (compounds D, F, G, and AB). Furthermore, the most effective antagonists (compounds C, L, M, N, P, Q, U, and V) also closely resemble the cognate autoinducer. However, there was little if any overlap in performance between effective agonists and the most effective antagonists. All agonists had acyl chains of seven carbon residues or more, and all had 3-oxo substituents. Therefore, TraR tolerated acyl groups one carbon shorter or up to four carbons longer than the cognate autoinducer and tolerated a triple bond at the 7-8 position but did not tolerate other alterations. In contrast, with one exception, the strongest antagonists lacked the 3-oxo substituent and had methylene residues, hydroxyl residues, or 2-3 unsaturated bonds at this position. The single best antagonist (compound M) is identical to the best autoinducer (compound E) except for the fact that compound M lacks the 3-oxo group. The exception to this pattern is compound C, which has a 3-oxo group but has a six-carbon fatty acyl group. Since antagonism is probably a consequence of competitive binding, we conclude that the 3-oxo group is completely dispensable for TraR binding but that it plays an important role in converting TraR into an active conformation.
Overproduction of TraR did not lead to constitutive expression of a
target promoter. Rather, promoter activity still required an
autoinducer, but the number of active compounds was
drastically increased. Overexpression of TraR therefore potentiated its
ability to activate transcription. Perhaps these data can best be
explained by postulating that autoinducers increase the
affinity of TraR either for other TraR monomers or for tra
box DNA (or conceivably for some other macromolecule such as RNA
polymerase). If so, autoinducer analogs may cause
similar but smaller increases in affinity. Small increases in affinity
would be insufficient to drive activation of wild-type TraR pools but
would be sufficient to cause activation when TraR is overproduced. To
help illustrate this point, we propose that 3-oxo-C8-HSL
may act by decreasing the Kd for TraR
dimerization from, perhaps, 104 to 107 M,
while 3-oxo-C6-HSL may decrease the
Kd to 106 M. According to this
hypothetical example, a low concentration of TraR (for example,
107 M TraR monomers) would permit significant
dimerization by 3-oxo-C8-HSL but not by
3-oxo-C6-HSL while a higher concentration of TraR (for example, 105 M TraR monomers) would permit significant
dimerization by both autoinducers. If
autoinducers decrease the Kd for
TraR-DNA or TraR-RNA polymerase interactions, very similar models can
be proposed.
There are at least two indications that active TraR is di- or oligomeric, as was previously suggested for LuxR (13). First, a truncated TraR-like protein lacking a DNA binding domain exerts dominant negative effects on tra gene expression, suggesting that it forms inactive heteromultimers (31, 47). Similar data have been reported for LuxR (7). Second, several putative TraR-binding sites show a strong dyad symmetry (16), suggesting that one monomer of a dimer contacts one arm of the dyad and that a second monomer makes identical contacts on the opposite arm.
Our observations are reminiscent of the data of Sitnikov and coworkers (41), who found that 3-hydroxy-C4-HSL failed to activate lux genes in V. fischeri but did so when the lux operon was cloned in E. coli, where LuxR may have been overexpressed. In the same study, C10-HSL was an antagonist of lux genes in V. fischeri but was an agonist in E. coli. Similarly, Schaefer and colleagues reported that 15 of 17 autoinducer analogs inhibited bioluminescence in V. fischeri (in the weakly bioluminescent strain B-61; see reference 13), while in a separate study, many of the same compounds did not inhibit bioluminescence in a recombinant strain of E. coli carrying a reconstituted lux regulon (37). Kuo and colleagues also demonstrated that C8-HSL is an antagonist in V. fischeri (28). LuxR was overexpressed in these E. coli strains, and this may have increased autoinducer sensitivity in a fashion similar to that observed for TraR in our study.
Similar studies have been carried out with an E. coli strain expressing LasR (32). In this study, LasR showed a broad substrate specificity, comparable to the response we observed using the TraR-overexpressing strain. Many of these compounds competed against radiolabeled 3-oxo-C12-HSL in a binding assay, but none interfered with induction of a target promoter. It is possible that LasR would have shown a narrower autoinducer specificity and would have been more effectively antagonized had it been expressed at wild-type levels. This may have important clinical implications, where autoinducer antagonists may be useful in treating Pseudomonas infections.
The ability of wild-type A. tumefaciens to discriminate between 3-oxo-C8-HSL and all other tested compounds should prevent induction by noncognate autoinducers released by other bacterial species. In fact, the only noncognate autoinducer that efficiently induced the tra regulon at low concentrations (3-oxo-C7-HSL) has an odd number of carbon atoms and is therefore unlikely to be found in nature. On the other hand, the finding that many compounds actively inhibited induction suggests that other bacterial species in the rhizosphere may interfere with autoinduction and thereby inhibit Ti plasmid conjugation. Whether this has important ecological consequences is not known. By analogy, one can imagine that 3-oxo-C6-HSL synthesized by A. tumefaciens may well perturb autoinduction by other bacterial species.
TraI can synthesize detectable amounts of several autoinducers in addition to 3-C8-HSL (Fig. 5). It is noteworthy that at least two of these compounds can inhibit induction of wild-type strains (Table 1). However, these compounds are synthesized at levels lower than that of 3-oxo-C8-HSL and are therefore unlikely to interfere with induction.
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ACKNOWLEDGMENTS |
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We thank the following Ithaca College chemistry students: L. David Finger for the synthesis of compounds H, AD, AE, and AG; Michael Kiefer for the synthesis of compounds Q, X, Z, AA, and AB; A. Damon for the synthesis of compounds S and W; and Anthony Atti, Adam Brownstein, Shomesh Doddi, J. P. Kirby, George Lemieux, Robert Lewis, Patrick Sarmiere, Jonathan Sparks, and Robert Tarsa for synthesis of compounds D, F, O, P, R, U, V, AC, and AF, respectively.
This study was supported by NIH grant GM42893.
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FOOTNOTES |
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* Corresponding author. Mailing address: Section of Microbiology, Cornell University, Ithaca, NY 14853. Phone: (607) 255-2413. Fax: (607) 255-3904. E-mail: scw2{at}cornell.edu.
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REFERENCES |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Journal of Bacteriology, October 1998, p. 5398-5405, Vol. 180, No. 20
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