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Báo cáo khoa học: The potyviral virus genome-linked protein VPg forms a ternary complex with the eukaryotic initiation factors eIF4E and eIF4G and reduces eIF4E affinity for a mRNA cap analogue ppt

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ternary complex with the eukaryotic initiation factorseIF4E and eIF4G and reduces eIF4E affinity for a mRNA cap analogue Thierry Michon, Yannick Estevez, Jocelyne Walter, Sylvie German-R

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ternary complex with the eukaryotic initiation factors

eIF4E and eIF4G and reduces eIF4E affinity for a mRNA

cap analogue

Thierry Michon, Yannick Estevez, Jocelyne Walter, Sylvie German-Retana and Olivier Le Gall Interactions Plante-Virus, UMR GDPP INRA-Bordeaux 2, Institut de Biologie Ve´ge´tale Mole´culaire, Villenave d’Ornon, France

Lettuce mosaic virus (LMV), is a member of the genus

Potyvirus [1] Potyviruses are plant viruses with flexible

rod-shaped particles packing a single-stranded,

poly-adenylated, positive-sense genomic RNA [2] This

RNA, of about 10 kb, is linked at its 5¢ end to a viral

protein, VPg (virus protein linked to the genome),

through a tyrosine phosphoester covalent bound [3–5]

The viral particle does not carry the molecular

machin-ery required for its replication in the host cell, and the

viral genome codes for a limited number of proteins

Thus the infectious cycle needs to recruit various host

factors, including the host translation apparatus

Eukaryotic mRNAs are capped by the addition of a

7-methylated guanine (m7G) This post-transcriptional

modification occurs in the nucleus [6,7] The 5¢-cap

acts as a flag on the mRNA for cytoplasmic export and for the ribosomal translation complex assembly The recognition of this m7G functional group by a cap-binding protein (eIF4E, the eukaryotic translation initiation factor 4E, or its isoform eIFiso4E) is the first step of a complex cascade of molecular events leading

to binding of the 40S ribosomal subunit to the mRNA [8] The general structural similarity between the poty-virus RNA and eukaryotic mRNAs suggests that VPg may act functionally as a cap-like structure This hypo-thesis gained strength when a specific interaction between eIF4E and VPg was identified in several patho-systems, such as tomato⁄ tobacco etch virus [9] and Arabidopsis thaliana⁄ turnip mosaic virus (TuMV) [10]

In the latter case, a single amino acid replacement in

Keywords

eIF4E; eIF4G; fluorescence; interaction; VPg

Correspondence

T Michon, Virologie Ve´ge´tale, GDPP,

IBVM-INRA, BP 81, 33883 Villenave

d’Ornon Cedex, France

Fax: +33 5 57 12 23 84

Tel: +33 5 57 12 23 91

E-mail: michon@bordeaux.inra.fr

Website: http://www.bordeaux.inra.fr/ipv/

(Received 10 October 2005, revised 23

January 2006, accepted 26 January 2006)

doi:10.1111/j.1742-4658.2006.05156.x

The virus protein linked to the genome (VPg) of plant potyviruses is a 25-kDa protein covalently attached to the genomic RNA 5¢ end It was previously reported that VPg binds specifically to eIF4E, the mRNAcap-binding protein of the eukaryotic translation initiation complex We per-formed a spectroscopic study of the interactions between lettuce eIF4E and VPg from lettuce mosaic virus (LMV) The cap analogue m7GDP and VPg bind to eIF4E at two distinct sites with similar affinity (Kd¼ 0.3 lm) A deeper examination of the interaction pathway showed that the binding of one ligand induces a decrease in the affinity for the other by a factor of 15 GST pull-down experiments from plant extracts revealed that VPg can specifically trap eIF4G, the central component of the complex required for the initiation of protein translation Our data suggest that eIF4G recruit-ment by VPg is indirectly mediated through VPg–eIF4E association The strength of interaction between eIF4E and pep4G, the eIF4E-binding domain on eIF4G, was increased significantly by VPg Taken together these quantitative data show that VPg is an efficient modulator of eIF4E biochemical functions

Abbreviations

BN, blue native; eIF4E, eukaryotic translation initiation factor 4E; GST, glutathione S-transferase; LMV, lettuce mosaic virus; PABP, poly(A)-binding protein; TuMV, turnip mosaic virus; VPg, virus protein linked to the genome.

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VPg abolished its interaction with eIF4E, and this

correlated with a defect in infectivity in Brassica

perviridis[11]

The simplest hypothesis is that VPg recruits eIF4E

to initiate the translation of the potyvirus polyprotein

[12] The involvement of eIF4E in pea seed-borne

mosaic virus cell to cell movement has been suggested

[13] Some lettuce cultivars display a recessive

resist-ance to LMV As this resistresist-ance is opposed by the

eIF4E isoform, we focused this study on the VPg–

eIF4E interaction [14] Whatever the biochemical

pro-cess involved, the VPg–eIF4E complex appears to play

a crucial role in the outcome of the plant–potyvirus

interaction Therefore, we developed a quantitative test

to (a) measure precisely the binding strength between

VPg and eIF4E and (b) assess the pathway of the

interactions between VPg, eIF4E and the cap structure

A glutathione S-transferase (GST) pull-down test from

plant extracts was used to demonstrate that VPg can

recruit the binary complex eIF4E–eIF4G, a component

of eIF4F, the complex of translation initiation Finally,

we evaluated the possible effect of VPg on eIF4G

binding to eIF4E using a synthetic peptide that

mimicks the eIF4G-binding domain

Results and discussion

Interaction between VPg and eIF4E

We initially evaluated the perturbation of the intrinsic

fluorescence of eIF4E upon its interaction with VPg

As VPg contains no tryptophan, the contribution of its

intrinsic fluorescence was assumed to be negligible with

respect to the nine tryptophans present in eIF4E

Upon the addition of VPg, a decrease in the overall

fluorescence of eIF4E was observed (Fig 1) This

seemed to correlate with a specific interaction between

the two proteins, as the fluorescence decrease reached

a plateau at high VPg concentrations The binding of

VPg only slightly affected eIF4E tryptophan

fluores-cence The signal-to-noise ratio was poor, implying

low accuracy in the determination of the dissociation

constant (Kd¼ 0.3 lm) The binding curve

extrapola-ted to a 1 : 1 stoichiometry for the two proteins

(Fig 1 inset)

From these data it is likely that VPg binding to

eIF4E is not associated with much modification of the

environment of the eIF4E tryptophans The two

tryp-tophan residues present in the cap-binding site are

accessible to the surface [15] Direct access of VPg to

the pocket would probably be associated with greater

modification of the fluorescence of these two residues,

as happens when cap analogues penetrate into the

pocket [16] The emission maximum of lettuce eIF4E was found to be at 342 nm, which is rather high It is likely that the major contribution to the intrinsic fluor-escence of the protein comes from these two trypto-phans in a polar environment, the fluorescence of the others being partially shielded This was also found in previous studies, although not to such an extent [16]

Binding-site characterization

To obtain a better fluorimetric response of eIF4E upon its interaction with VPg, we attempted to follow indi-rectly the complex formation using the cap analogue

m7GDP There are considerable discrepancies between the affinities of the cap analogue published so far In the absence of VPg, the value of the dissociation constant obtained (Kc¼ 0.31 ± 0.02 lm) was significantly lower than in previous reports for this type of analogue [17,18] A possible explanation is that, during the proce-dure used for eIF4E isolation, the elution step from

m7GTP–Sepharose 4B is usually performed with free

m7GTP We observed that, even after extensive dialysis,

a significant fraction of active eIF4E retains m7GTP

in its binding site (data not shown) In our study, all eIF4E fractions were previously eluted from m7GTP– Sepharose 4B with 1 m KCl instead of m7GTP (see Experimental Procedures) However, it cannot be exclu-ded that lettuce eIF4E displays a higher affinity for the

Fig 1 Fluorescence emission spectra of eIF4E upon VPg addition Aliquots of 2.5 lL from a 60-l M VPg stock solution were added

to a 0.5-l M eIF4E solution in buffer M After each addition, the mixture was incubated for 5 min at 25 C, and spectra were recor-ded (- - - -) No VPg added; (—) from top to bottom increasing amounts of VPg Inset: variation in eIF4E fluorescence as a function

of VPg concentration in the medium.

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cap than its wheatgerm counterpart It is worth

men-tioning that, in a recent study, values in the nanomolar

range were reported The authors emphasize that this

could be because the recombinant eIF4E used was

obtained from carefully renatured batches from

inclu-sion bodies [19], thus avoiding affinity purification

involving exposure to cap analogues

The apparent dissociation constant of m7GDP to

eIF4E was higher in the presence of increasing

amounts of VPg (Fig 2) The plateau value (ligand

saturation) was also affected (Fig 2, inset) It was

sus-pected that VPg could remain bound to eIF4E even at

high cap analogue concentrations The fact that

m7GDP could not displace VPg argued in favour of

the presence of a VPg-binding site on eIF4E, which is

distinct but structurally related to the cap-binding site

A possible mixed-type noncompetitive ligand binding

of eIF4E and the cap to the VPg was reported

previ-ously [11] However, as the amount of free and bound

ligand was not determined, a nonlinear

double-recipro-cal plot was obtained, from which it was difficult to

establish an accurate pathway for the interactions [20]

Complexes between proteins often involve large

sur-face overlaps It cannot be ruled out that VPg interacts

with eIF4E through several domains, one of them being structurally linked to the cap site In such a case, the presence of VPg might negatively affect the binding

of m7GDP To discriminate between competitive and noncompetitive interactions, we performed a m7GDP– eIF4E binding test in the presence of a large excess of VPg (30–60 lm) with respect to eIF4E (2 lm) In such conditions, the concentration of free VPg ([V]free) is assumed to be close to [V]total The same saturation behaviour was observed as for lower concentrations of VPg (Fig 3A) In the case of strict competition, the

Fig 2 Effect of VPg on m 7 GDP binding to eIF4E at 25 C VPg

aliquots were mixed with 2 l M eIF4E in buffer M Before titration

with m 7 GDP Inset: isotherms of m 7 GDP binding to eIF4E Solid

lines represent theoretical data calculated using the best fit of the

experimental data to eqn (4) (see Experimental Procedures) (d) No

VPg; (s) 0.3 l MVPg; (n) 1.2 lM VPg; (h) 2.4 l M VPg.

Fig 3 (A) Binding isotherms of m 7 GDP with eIF4E in the presence

of high VPg concentrations Experimental conditions were as in Fig 2 Lines represent theoretical data calculated using the best fit

of the experimental data to eqn (4) using either two distinct but dependent sites (solid line) or strict competition at the same site (dashed line) All measurements were made at least in triplicate (d) 30 l M VPg; (s) 60 l M VPg (B) Plots of residuals between the-oretical and experimental data using either two distinct but depend-ent sites (solid line) or strict competition at the same site (dashed line) VPg concentration, 30 l M

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apparent dissociation constant Kapp

c can be derived according to Scheme 1A as:

Kcapp¼ Kc 1þ½Vfree

Kv

ð1Þ

where [V]free is the concentration of free VPg in the

medium

The apparent dissociation constant for binding at

two distinct but dependent sites defined in Scheme 1B

is:

Kcapp¼ Kc

Kvþ ½Vfree

Kvþ½Vfree

a

!

ð2Þ

where a and KV are the ratio of symmetrical

dissoci-ation constants (Scheme 1B) and the VPg–eIF4E

disso-ciation constant, respectively

In this case, as eIF4E remains partitioned between

the three species eIF4E–m7GDP, m7GDP–eIF4E–VPg,

and eIF4E–VPg whatever the concentration of

m7GDP, the plateau value is also affected and:

Ysatapp¼ Ysat

Kv

aKvþ ½Vfree

ð3Þ

Kcand Ysatwere replaced in eqn (4) by the expressions

Kapp

c and Ysatapp Assuming [V]free to be close to [V]tot,

data sets of eIF4E fluorescence as a function of

[m7GDP]total were fitted to models mimicking either

strictly competitive binding or binding at two distinct

but dependent sites Plots of residuals obtained from both fits showed unambiguously that VPg and m7GDP bind to distinct but interdependent sites (Fig 3B) Although the cap analogue and VPg displayed com-parable affinity for eIF4E (Kc¼ 0.31 ± 0.02 lm and

Kv¼ 0.3 ± 0.03 lm), binding of the first molecule affected the binding of the second one by a factor 15 (a¼ 15 ± 3) We examined the effect of disruption of the cap-binding capacity on eIF4E association with VPg To do so, we engineered W123A, an eIF4E mutant in which W123, one of the two conserved tryp-tophan residues involved in p-p stacking with the cap aromatic moiety [15], was substituted with an alanine

As expected, this substitution abolished m7GDP bind-ing to W123A while retainbind-ing its capacity to associate with VPg (Table 1) The VPg surface defining the zone

of interaction with eIF4E spans at least two distinct domains, one of which can affect the topology of the cap-binding pocket The VPg–eIF4E interaction may

be a mechanism for recruiting the host translation machinery cut off by several unrelated positive-stran-ded RNA viruses In a recent study, an interaction between VPg and a human enteric calcivirus was dem-onstrated [21]

GST pull-down assay of plant proteins forming complexes with VPg

Several studies have reported specific interactions between the VPg from potyvirus and eIF4E or one of its isoforms [9] A recombinant VPgÆGST fusion pro-tein was used as a bait for trapping molecular species susceptible to be recruited by VPg in planta A soluble protein fraction was recovered after mild detergent treatment of the plant leaves This extract was submit-ted to a VPgÆGST pull-down procedure [22] To deter-mine the nature of the protein complexes involved in specific interactions with VPg, the fraction recovered was analysed by electrophoresis in native conditions A high-molecular-mass (above 200 kDa) species and two minor species (below 100 kDa) were affinity-purified from the protein extract (Fig 4A, lane 2) A western blot analysis with antibodies to VPg showed that all

Table 1 Equilibrium association constants for various forms of eIF4E and its ligands NB, no binding detected.

Kc

VPg

eIF4E-VPg

Kv

m 7 GDP

A

VPg-eIF4E-m 7 GDP

αK v

αK c

B

VPg

Kc

m 7 GDP

VPg

eIF4E-VPg

Kv

m 7 GDP

Scheme 1 Two plausible models for the interactions between

eIF4E, VPg and the cap analogue 7 mGDP (A) Strictly competitive

model; (B) binding at two distinct but dependent sites.

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contained this protein (Fig 4A, lane 3) As the

inter-action of VPg with plant translation initiation factors

was suspected, a western blot was performed with

spe-cific antibodies to eIF4E (lane 4) and eIF4G (lane 5)

Two of the three species (the one >205 kDa and the

intermediate one) contained eIF4E (lane 4) The eIF4G

forms were restricted to the high-molecular-mass

spe-cies (lane 5) When pull-down assays were performed

on extracts from infected leaves, the highest-molecular-mass species was not detected (lane 6)

The purified fraction was also analysed by SDS⁄ PAGE to determine the composition of the com-plexes They mainly contained three groups of poly-peptide chains according to their relative molecular masses: a group with bands in the range of 180 kDa, a 54-kDa band, and a single chain of 26 kDa (Fig 4B, lane 4) The proteins were identified by western blot-ting Antibodies to eIF4G revealed many polypeptides

in the 70–200 kDa region (Fig 4B, lane 5) It has pre-viously been reported that, in several organisms, eIF4G is highly susceptible to proteolysis [23] It is likely that, during the extraction step, cleavage occurred along the polypeptide chain Whereas blue native (BN)-PAGE native conditions revealed a single molecular species probably because of conformational locking, SDS⁄ PAGE denaturing conditions revealed the proteolysis

The VPg antibodies reacted with a single 54-kDa polypeptide corresponding to the GSTÆVPg fusion (Fig 4B, lane 6) The eIF4E antibodies revealed only a 26-kDa polypeptide in accordance with the expected plant eIF4E (Fig 4B, lane 7) Our GST pull-down experiment showed that VPg can recruit eIF4E (26 kDa [14]) and eIF4G ( 180 kDa according to

A Thaliana eIF4G [24]) From the SDS⁄ PAGE pattern we could determine precisely the nature of the three complexes revealed by BN-PAGE analysis The highest-molecular-mass band (>205 kDa) corres-ponds to the heterotrimer eIF4G–eIF4E–VPgÆGST ( 260 kDa; Fig 4A, compare lanes 3, 4 and 5) The intermediate band ( 80 kDa) observed in native conditions contained VPg and eIF4E but not eIF4G (Fig 4A, compare lanes 3 and 4 with 5) It was attributed to the binary complex GSTÆVPg–eIF4E The band of lowest molecular mass,  54 kDa, on BN-PAGE was unambiguously identified as the GSTÆVPg fusion on SDS⁄ PAGE (Fig 4B, lane 6; see also lane 2 for comparison with pure GSTÆVPg)

We demonstrate here that the VPg–eIF4E interac-tion previously described in other pathosystems such

as TuMV⁄ B perviridis is also found in the LMV ⁄ let-tuce system However, this is the first report of a phys-ical interaction between VPg and eIF4G At this stage,

we found no evidence for a direct interaction between VPg and eIF4G The recruitment of eIF4G by VPg is probably indirectly mediated by eIF4E as the central element of the complex This should display at least two distinct binding sites, one for VPg and the other for eIF4G In control experiments, the protein extract was incubated with unfused GST before the affinity chromatography GST alone failed to pull down any

A

B

Fig 4 Analysis of the plant soluble proteins complexed with VPg.

(A) BN-PAGE of the protein fraction retained on

glutathione–Seph-arose 4b Lane 2, the plant soluble extract was incubated with

recombinant VPgÆGst fusion and mixed with

glutathione–Seph-arose 4b beads After extensive washing, the proteins specifically

retained on the resin were eluted with glutathione (see

Experimen-tal procedures for details) The fractions obtained were loaded on

to a 6–18% polyacrylamide slab gel After migration, the complexes

were Coomassie stained Proteins from lane 2 were transferred to

a nitrocellulose membrane Complexes were revealed with

poly-clonal antibodies raised against VPg (lane 3), eIF4E (lane 4) and

eIF4G (lane 5) Lane 6, same as lane 2 except that protein extracts

were from LMV-Infected plants (40 lg VPgÆGst added) (B)

Sds ⁄ PAGE of the proteins retained on glutathione–Sepharose 4b.

Affinity chromatography was as in (A) Lane 4, electrophoretic

pat-tern of the protein fraction under denaturing conditions; Coomassie

blue staining Lanes 5, 6 and 7: Western blot analysis of the

pro-teins retained using polyclonal antibodies raised against eIF4G, VPg

and eIF4E, respectively Lane 1, molecular mass markers Lane 2:

recombinant GSTÆVPg fusion extracted from E coli and

affinity-purified on glutathione–Sepharose 4b Lane 3, as a control, the plant

soluble extract was incubated with nonfused recombinant GST

and mixed with glutathione–Sepharose 4b After being washed,

the fraction eluted with glutathione was analysed By SDS ⁄ PAGE.

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other species from the plant extract, confirming that

the formation of specific complexes with eIF4E and

eIF4G only involved the VPg domain of the GSTÆVPg

fusion (Fig 4B, lane 3) In another set of experiments,

the GSTÆVPg pull-down was challenged by mixing

increasing amounts of pure recombinant VPg with the

plant extracts The presence of VPg weakened the

interactions between the bait and eIF4E (Fig 5A) To

study the interaction in the context of infection,

extracts from LMV-infected plants were incubated

with increasing amounts of purified GSTÆVPg before

affinity chromatography on glutathione–Sepharose 4B

A 10-fold excess of GSTÆVPg was necessary to recover

an amount of eIF4E–GSTÆVPg complex comparable to

that observed from uninfected plants (Fig 5B)

GSTÆVPg may be strongly challenged by the presence

of viral VPg forms involved in complexes with the

ini-tiation factors in planta A very small amount of free

eIF4E may be accessible to GSTÆVPg, most of it

asso-ciated with the viral form It was not possible to detect

the eIF4E–eIF4G complex from infected plant extracts

whatever the amount of GSTÆVPg added (Fig 4A,

lane 6) If VPg binds strongly to the binary complex

eIF4E–eIF4G, it may hardly be displaced by

GSTÆVPg Moreover, VPg can exist in several

molecu-lar forms in the infected cell Sequential processing of

the polyprotein may be linked to a specific requirement

during each phase of the viral cycle Of the molecular

forms of VPg, 6K2ÆVPgÆPro and VPgÆPro copurify with

eIF4E in complexes associated with membrane

frac-tions [25] In infected cells, a substantial amount of

eIF4G may be involved in complexes with endogenous

forms of VPg If these complexes are tightly bound to

membranes, they may be less efficiently extracted

under our conditions

The strength of interaction between elF4E and pep4G, the eIF4E-binding domain on eIF4G, is enhanced by VPg

The eukaryotic eIF4F initiation complex is a hetero-trimer consisting of eIF4E, eIF4A (an RNA helicase) and eIF4G [26] In mammals, the central part of eIF4G contains three evolutionary conserved hydro-phobic amino acids, a tyrosine and two consecutive leucines separated by four less well conserved residues (YxxxxLL) This motif is associated with eIF4E bind-ing [27] Small oligopeptides that mimick this eIF4E recognition motif can bind to eIF4E This recognition motif is also highly conserved in the plant kingdom The lettuce eIF4G sequence is not available Knowing the high homology of this sequence between wheat (Q03387) and A thaliana (NP567095), the oligopeptide KKYSRDFLLKF from A thaliana (pep4G) was synthesized and tested for its ability to bind to lettuce eIF4E In the mammalian 3D structure, Trp73 is in close contact with the peptide [28] Lettuce eIF4E was modelled on the basis of its homology with the known structure of its mammalian counterpart [14] We hypo-thesized that the fluorescence of Trp94 (Trp73 in mouse) may be affected by pep4G binding This fea-ture has been used successfully to monitor pep4G binding to murine eIF4E [19] When eIF4E was incu-bated either alone or after saturation with VPg, a fluorescence decrease proportional to the amount of complex formed was observed, leading to a saturation plateau (Fig 6) Interestingly the strength of binding

of pep4G to the preformed eIF4E–VPg complex (Kd¼ 0.083 ± 0.016 lm) was significantly higher than that to the free eIF4E (Kd¼ 0.24 ± 0.03 lm) The reciprocal was not observed, as there was no effect of increasing concentrations of pep4G on the binding strength between VPg and eIF4E (Fig 6 inset) As found above for VPg and m7GDP, one could expect the interdependence of VPg and pep4G with respect to their binding to eIF4E It cannot be ruled out that the association of VPg with eIF4E induces a change in its conformation, enhancing the fit of the eIF4E-binding domain to pep4G The interaction of VPg with eIF4E affects the properties of both the cap-binding pocket and the eIF4G-binding domain Our observation is consistent with VPg–eIF4E interactions mediated over

a large area Long-range effects on the conformation

of eIF4E probably occur upon VPg binding The data should be interpreted with caution, as we cannot pre-sume that the effect of VPg is the same for binding of whole eIF4G The association of pep4G with eIF4E has been shown not to be accompanied by detectable changes in the crystallographic structure of eIF4E [28]

Fig 5 (A) Competition experiments with the recombinant VPg The

plant soluble extract was incubated with recombinant VPgÆGst

fusion in the presence of 10 lg (lane 2) and 50 lg (lane 3) of pure

recombinant VPg; lane 1, no VPg added After affinity

chromatogra-phy on glutathione–Sepharose 4b, the proteins were submitted To

BN-PAGE and analysed by western blotting with polyclonal

anti-eIF4E (B) LMV-Infected plant extracts were incubated with

increas-ing amounts of recombinant GSTÆVPg fusion before affinity

chroma-tography Proteins were analyzed by western blotting with

polyclonal antibodies against eIF4E Lane 1, 10 lg VPgÆGst fusion;

lane 2, 30 lg VPgÆGst fusion; lane 3, 60 lg VPgÆGst fusion; lane 4,

100 lg VPgÆGst fusion; lane 5, 150 lg VPgÆGst fusion.

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In fact, pep4G has a small effect on cap binding,

whereas whole eIF4G is a strong enhancer of eIF4E

binding to the mRNA cap structure [29] A

thermody-namic analysis predicts that the cocrystal structure of

the pep4G–eIF4E complex encompasses most of the

energetically significant interactions between eIF4G

and eIF4E [28] However, more recently, an NMR

structure of the binary complex between yeast eIF4E

and the eIF4G (393–490) domain was analyzed It

shows unambiguously that the N-terminus of eIF4E,

which interacts with the eIF4G domain, promotes

dis-creet conformational changes in the cap-binding site,

allowing tighter binding of the cap [30] The

thermo-dynamic parameters expressed as association constants

are tabulated for comparison (Table 1) VPg is an

efficient modulator of eIF4E properties Scheme 2

summarizes a hypothetical distribution of the initiation

factors eIF4E and eIF4G according to the

thermo-dynamic binding strengths measured in this study

In early stages of infection, the only form of VPg

present in the host cell is linked to the viral genome

Its concentration is low compared with the

concentra-tion of host cap mRNAs If VPg affinity in vivo is of

the same order of magnitude as in vitro, it is unlikely

that it will recruit eIF4E by displacing eIF4E–mRNA complexes Instead, the newly uncoated VPg–RNA molecules will require free eIF4E to start translation and⁄ or other steps of the virus cycle It is likely that the pull-down experiment on healthy plant extracts reveals only eIF4E and eIF4G forms that are not involved with cellular mRNA As translation proceeds, the amount of VPg increases in the infected cell The stoichiometry of the viral particle assembly is of the order of 2000 capsid proteins for one VPg [31] There-fore, the synthesis and proteolytic maturation of the polyprotein lead to a considerable excess of VPg over that strictly required for virion assembly According to our data, the association of VPg with free eIF4E should enhance its affinity for eIF4G This would account for the inability of the VPgÆGST fusion to dis-place viral VPg Most of the newly synthesized VPg may recruit free eIF4E and possibly eIF4G, thereby exerting a negative co-operative effect on the binding

of cellular mRNAs [32] As eIF4E is the limiting factor for translation efficiency [33], such sequestration may affect host cell metabolism and perhaps contribute to disease symptoms A large amount of the VPg–Pro form accumulates in the nucleus as nuclear inclusions,

in relation to a functional nuclear localization signal present in the Pro domain [34] In animal cells, a signi-ficant proportion of eIF4E itself is located in the nuc-leus [35] If this is also true in plants, retention of initiation factors in the nucleus through interaction with nuclear VPg may contribute to depletion of the cytoplasmic pool of free eIF4E, and disrupt mRNA translation In turn, the host cell may respond to this disruption by increasing the expression of another eIF4E isoform, as shown in B perviridis after infection with TuMV [25]

In eukaryotes, translation initiation of cellular mRNAs is mediated through the closed loop model connecting the capped 5¢ end of the messenger to its polyadenylated 3¢ end Circularization is thought to

Fig 6 Effect of VPg on the association between eIF4E and pep4G.

(s) Titration of free eIF4E by pep4G (d) The formation of the

tern-ary complex VPg–eIF4E–pep4G was monitored after a prelimintern-ary

titration of eIF4E with VPg up to saturation (eIF4E concentration

2 l M , VPg final concentration 5 l M ) Inset: (d) The apparent

dis-sociation constant K dapp of eIF4E–pep4G was determined in the

presence of increasing amounts of VPg (s) The apparent

dissoci-ation constant K dappof eIF4E–VPg was determined in the presence

of increasing amounts of pep4G.

VPg eIF4E ⇔ eIF4E-cap

eIF4E-VPg cap-eIF4E-VPg

VPg

eIF4G-eIF4E-cap

Scheme 2 Hypothetical pathways of eIF4E and eIF4G recruitment Large arrows highlight the connections that, according to the experimental data, would be thermodynamically favoured.

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increase translation efficiency by facilitating de novo

initiation and recycling of terminating ribosomes on

the same mRNA [36] The 3¢ polyadenylated end of

mRNAs is bound to the poly(A)-binding protein

(PABP) Circularization of the potyvirus RNA could

be achieved through the 5¢ VPg instead of the cap

structure The VPg–eIF4E–eIF4G–PABP complex

would bring together the 3¢ poly(A) and the 5¢ VPg

ends of the viral RNA As it has been reported that

VPgÆPro from TuMV can bind to PABP [25], another

possibility is that circularization is achieved through

VPgÆPro–PABP, this more direct binding skipping the

eIF4G–PABP interaction [37] Both mechanisms may

be present at different stages of the virus cycle It is

likely that viral recruitment of the 40S ribosome

sub-unit is mediated by the eIF3–eIF4G–eIF4E interaction

as for cellular mRNAs (see [38] for a review of

trans-lation initiation factors) Although there is no evident

internal ribosome entry site in the 5¢ part of the LMV

genome, the possibility of internal positioning of the

ribosome was demonstrated using an uncapped

tobacco etch virus 143 nucleotide leader It has been

shown that, in such conditions, translation still

requires eIF4G [39] Taken together, the data

presen-ted here strengthen the hypothesis of a physical

involvement of eIF4G in the translation initiation

complex of LMV

Experimental Procedures

Materials

Desalted water was further purified using a Q

were from Sigma Aldrich (Lyon, France) All solutions

were filtered through a 0.22-lm membrane before use The

peptide pep4G was synthesized by a solid-phase method

using F-moc chemistry [40] and purified by reversed-phase

after injection with purified recombinant proteins

Protein expression and isolation

The gene coding for the eIF4E was cloned from the lettuce

(Lactuca sativa) cultivar Salinas AAP86602, which is

sus-ceptible to LMV [14] The VPg coding sequence was

PCR-amplified from a partial LMV cDNA (isolate LMV-0,

P31999) cloned in Escherichia coli Both cDNAs were

inserted into the pTrcHis-C expression vector (Invitrogen)

in-frame with an N-terminal hexahistidine tag, according to

the manufacturer’s instructions The W123A mutant of

Mutagenesis Kit developed by Stratagene E coli (strain

BL21) was transformed with pTrcHisC-eIF4E or pTr-cHisC-VPg Overnight Luria–Bertani broth starters were

Luria–Bertani broth containing ampicillin were inoculated with 50 mL of the overnight culture starter and grown at

addition of 0.5 mm isopropyl b-d-thiogalactoside, and cells

DNA sequences encoding GST and GSTÆVPg fusion were

(Invitrogen) The expression vectors were introduced into

arabinose, the expression vector was run in the same condi-tions as above All proteins were submitted to the same

Phenylmethanesulfo-nyl fluoride (100 lL of a 200-mm stock solution in meth-anol) was added at each step of the extraction Cells were centrifuged and suspended in 30 mL HEX buffer (20 mm

added, and the suspension was incubated for 45 min at

another 45 min The lysate was sonicated in ice for

3 min (1 s cycles) The crude extract was centrifuged at

buffer The beads were centrifuged at low speed and packed into a 2 mL column The beads were washed with HEX

con-stant value Proteins were eluted by a 10–250 mm imidazole

fractions containing proteins was pooled

Specific isolation procedures

After being desalted, VPg fractions were refined by

mono Q column (Amersham Biotech) Pure VPg was

recovered from ion metal affinity chromatography were

dithiothre-itol was added to achieve a final concentration of 100 mm

100 mm KCl, 1 mm dithiothreitol) The beads were centri-fuged at low speed, packed into a 2-mL column, and washed with buffer A Protein elution was performed with

Trang 9

1 m KCl in buffer A After SDS⁄ PAGE analysis, the

fractions containing eIF4E were pooled and concentrated

under nitrogen on an Amicon ultrafiltration cell equipped

with a YM10 membrane (Millipore) After being desalted,

Protein concentration was determined

VPg, respectively GST and GSTÆVPg fusions were

affinity-purified on glutathione–Sepharose 4B beads (Amersham

Bioscience) as described in the following section

Pull-down assays

Fresh leaves (1 g) were frozen in liquid nitrogen and

ground The powder was suspended in 2 mL cold HEX

buffer Then 10 lL 200 mm phenylmethanesulfonyl fluoride

stock solution in methanol and 25 lL Sigma P8340

prote-ase cocktail inhibitor were added The suspension was

fil-tered through glass wool The filtrate was centrifuged at

fluor-ide and protease cocktail inhibitor were added Typically

2.5 mg soluble proteins were recovered by this procedure

The extract was incubated with 100 lL

super-natant was mixed with 100 lL glutathione–Sepharose 4B

beads, and 1 mL fractions were incubated with either 10 lg

recovered and washed extensively with ice-cold HEX buffer

The proteins were eluted with 100 lL 10 mm reduced

10 lL were used for PAGE analysis BN-PAGE was

car-ried out using 6–18% polyacrylamide slab gels as described

previously [41] Proteins were revealed by western

immuno-blotting with specific polyclonal antibodies

Fluorescence measurements

spectrophotometer (Monaco) Excitation and emission slits

were set to a 10-nm path The photomultiplier’s power was

set at 600–800 V (of a maximum possible value of 1200 V)

The photons emitted were collected at right angles from the

vertical excitation beam The geometry of the device

allowed us to set the optical path length of the emitted light

1 mm above the excitation source With this set-up,

fluores-cence emission was linear up to 0.7 absorbance units at the

wavelength of excitation (data not shown) The excitation

wavelength was set at 258 nm Although there is a

optical system the inner filter effect was about 2% at the

highest concentration and no correction was made By

exci-ting the sample at 258 nm, the Raman peak contribution to the emission spectrum was prevented In water, Raman

In the buffer used, the excitation at 258 nm was accompan-ied by a Raman peak at 282 nm, which was far from the maximum of emission observed (343 nm) The nine trypto-phan residues in eIF4E make the intrinsic fluorescence important, allowing the recovery of a very good signal even when exciting at 258 nm

These conditions proved in preliminary experiments to give the best ratio of signal to noise for the observation of tryptophan fluorescence quenching at 342 nm This set-up was in accordance with the original studies of eIf4E titra-tion with cap analogues [16,42] Measurements were made

1 mm dithiothreitol and 10% glycerol) The concentration

of eIF4E was between 0.5 and 2.5 lm Ligand stock solu-tions were adjusted in such a way that the volume added upon titration never exceeded 5% of the total volume After addition of the ligand, emission at 342 nm was recor-ded over a period suitable for reaching a constant fluores-cence value (steady-state usually after 5 min) The decrease

in fluorescence with respect to the initial fluorescence was recorded, and corrections were made for dilution BSA was used as a control under the same conditions to test for nonspecific binding The fluorescence signal did not show significant changes upon BSA Addition (data not shown)

In some experiments, it was necessary to perform emission measurements in the presence of high VPg concentrations Quantum yield loss was estimated according to the equation

Fcor¼ Fobs 10ð0:5AexÞ

correc-ted and observed, and Aex is the absorbance of the solution

at 258 nm [43] As the quantum yield decrease was less than 3%, no inner filter correction was necessary VPg emission was checked at high VPg concentration No significant light scattering was observed For each ligand concentration, three data acquisitions were made

Data analysis

Let us consider the simple bimolecular association between eIF4E and one ligand:

Kc EC According to this scheme, the saturation function of eIF4E with its ligand follows an hyperbola:

The experimental procedures used in this work do not allow direct determination of bound and free ligand concentrations without access to [Ec] and [C] eIF4E fluorescence decreases together with the eIF4E–ligand

Trang 10

complex formation The association is followed by

For the sake of comparison between various sets of data,

Ysat

ð5Þ Eqn (1) becomes:

½C

An interesting feature of eqn (6) is that it expresses a

sat-uration function that does not require the true



ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi

Kcþ ½Ctotþ Ysat

 4½CtotYsat

q

ð7Þ Hypothetical models of interaction were examined by fitting

the associated equations to experimental data using

non-linear regression Affinity constants were determined from

the model giving the best fit to the data

Acknowledgements

We would like to thank Genevieve Roudet for her

skil-ful assistance, and Dr T Candresse and Dr T

Delau-nay for stimulating discussions Many thanks to

Professor K S Browning for providing us with eIF4G

polyclonal antibodies We thank Dr J F Bussotti

from SAFAS S.A for his skilful assistance in optical

device optimization We are grateful to C Manigand

(UMR 5471 CNRS-Bordeaux 1) for pep4G synthesis

We are indebted to region Aquitaine for its financial

support for this work

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