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Water and glycerol permeability of wild-type BccGlpF and mutants To test for water permeability, we expressed wild-type BccGlpF and mutants in a yeast strain that lacked the endogenous a

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sequence signature motifs for cation exclusion

Dorothea Wree1, Binghua Wu1, Thomas Zeuthen2and Eric Beitz1

1 Department of Pharmaceutical and Medicinal Chemistry, Christian-Albrechts-University of Kiel, Germany

2 Institute of Cellular and Molecular Medicine, University of Copenhagen, Denmark

Introduction

Aquaporins (AQPs) of the orthodox, water-specific

subfamily and of the water-permeable and

solute-per-meable aquaglyceroporin subfamily share a common

protein fold [1] It comprises six membrane-spanning

helices plus two half-helices with their positive,

N-ter-minal ends located at the centre of the protein and

their C-terminal ends pointing towards either side of

the membrane The helices surround the 20-A˚-long

and 3–4-A˚-wide amphipathic AQP channel Two

con-served constriction sites are present in the channel The aromatic⁄ Arg (ar ⁄ R) constriction is located at the extracellular pore mouth Its diameter determines whether or not solutes, such as glycerol and methyl-amine, can pass the AQP in addition to water [2–5] Furthermore, the positively charged residues in this region form an energy barrier for protons [2,3,5] The role in pore selectivity of the ar⁄ R constriction is well understood, owing to several theoretical and

Keywords

aquaglyceroporin; aquaporin; potassium;

proton; sodium

Correspondence

E Beitz, Pharmaceutical Institute,

Christian-Albrechts-University of Kiel,

Gutenbergstrasse 76, 24118 Kiel, Germany

Fax: +49 431 880 1352

Tel: +49 431 880 1809

E-mail: ebeitz@pharmazie.uni-kiel.de

Website: http://www.pharmazie.uni-kiel.de/

chem/

(Received 8 November 2010, revised 10

December 2010, accepted 13 December

2010)

doi:10.1111/j.1742-4658.2010.07993.x

Two highly conserved NPA motifs are a hallmark of the aquaporin (AQP) family The NPA triplets form N-terminal helix capping structures with the Asn side chains located in the centre of the water or solute-conducting channel, and are considered to play an important role in AQP selectivity Although another AQP selectivity filter site, the aromatic⁄ Arg (ar ⁄ R) con-striction, has been well characterized by mutational analysis, experimental data concerning the NPA region – in particular, the Asn position – is miss-ing Here, we report on the cloning and mutational analysis of a novel aquaglyceroporin carrying one SPA motif instead of the NPA motif from Burkholderia cenocepacia, an epidemic pathogen of cystic fibrosis patients

Of 1357 AQP sequences deposited in RefSeq, we identified only 15 with an Asn exchange Using direct and phenotypic permeability assays, we found that Asn and Ser are freely interchangeable at both NPA sites without affecting protein expression or water, glycerol and methylamine ity However, other mutations in the NPA region led to reduced permeabil-ity (S186C and S186D), to nonfunctional channels (N64D), or even to lack

of protein expression (S186A and S186T) Using electrophysiology, we found that an analogous mammalian AQP1 N76S mutant excluded protons and potassium ions, but leaked sodium ions, providing an argument for the overwhelming prevalence of Asn over other amino acids We conclude that, at the first position in the NPA motifs, only Asn provides efficient helix cap stabilization and cation exclusion, whereas other small residues compromise structural stability or cation exclusion but not necessarily water and solute permeability

Abbreviations

AQP, aquaporin; ar ⁄ R, aromatic ⁄ Arg; BccGlpF, Burkholderia cenocepacia glycerol facilitator; Ch, choline; EcGlpF, Escherichia coli glycerol facilitator; HA, haemagglutinin.

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experimental studies, which have elucidated

contribu-tions of the individual residues at this site The second

constriction resides in the centre of the channel, where

the positive ends of the two half-helices meet The helix

dipole moments add up to a full positive charge, and

the resulting electrostatic field poses another energy

barrier for cations [6] The residues that constitute the

capping structures of the half-helices are extremely well

conserved in the two canonical NPA motifs Although

there is some degree of variation in the second and

third positions [7–9], the Asn at the first position

appears to be almost invariable [10,11] The Asn side

chain amide moieties fulfil two roles: (a) the carbonyl

oxygens form hydrogen bonds with backbone nitrogen

atoms of the preceding two amino acids, stabilizing the

helix cap; and (b) the amide nitrogens act as hydrogen

bond donors to passing water or solute molecules, and

may thus be involved in AQP selectivity

We identified, in the genomes of Burkholderia sp

[12], genes encoding aquaglyceroporins that

intrinsi-cally have SPA at the second NPA motif position The

natural occurrence of an Asnfi Ser exchange led us

to analyse the functional consequences of Asn

replace-ments at the NPA sites by site-directed mutagenesis

As expected, we found that the Asn positions are

structurally critical However, the Asn positions in

both NPA motifs can be occupied by Ser, yielding

functional AQPs with unaltered water and solute

permeability However, Ser leads to a sodium leak

in mammalian AQP1, which may explain why 99% of

all AQPs carry Asn at the NPA sites

Results

Natural replacement of Asn in the NPA motifs is

rare

Inspection of the b-proteobacterial genome data from

Burkholderia species, i.e Burkholderia cenocepacia [12],

Burkholderia cepacia, Burkholderia mallei,

Burkholde-ria pseudomallei, and BurkholdeBurkholde-ria fungorum, yielded a

family of putative aquaglyceroporin genes encoding

proteins with unusual NPA motifs (Fig S1) The

sec-ond NPA motif appeared to be altered to SPA,

whereas the remaining sequences were 38% identical

and 58% similar to the prototypical aquaglyceroporin

from Escherichia coli [E coli glycerol facilitator

(EcGlpF)] [13] We then analysed 1357 AQP sequences

deposited in the RefSeq database [14], and identified

only 15 (1.1%) with a substitution of one of the Asn

residues in the NPA motifs by Ser or Cys, which is in

line with the findings of an earlier study [11] A

fre-quency-corrected sequence logo [15] shows the strong

conservation of the NPA motifs and of the direct sequence vicinity (Fig 1A, top) To search for addi-tional characteristic amino acid exchanges in the Burk-holderia aquaglyceroporin subfamily, we generated a subfamily logo [16], which displays sequence deviations

at alignment positions with high information content, i.e at conserved positions The result for the NPA regions is shown in Fig 1A (lower panel) Residues of the subfamily are displayed upright, whereas residues

of the remaining set of proteins appear upside-down

A

B

Fig 1 Sequence comparison and structure model of the NPA ⁄ SPA region of BccGlpF (A) The upper panel depicts a sequence logo of the AQP family, showing conservation of the five residues upstream and downstream of the Asn position of either NPA motif (labelled with black bars) The subfamily logo [16] below indicates residues that are characteristic for the Burkholderia aquaglyceropo-rin subfamily (upright symbols), and the upside-down letters indi-cate the corresponding residues of the remaining set of AQPs The more distinct a residue, the more information is contained at this site, as reflected by the height of the symbol The actual BccGlpF sequence is given below the logos (B) Structural model of the BccGlpF NPI-SPAR sequence region based on EcGlpF (Protein Data Bank: 1FX8) [13] Asn64, Ser186 Arg189 and the indicated carbonyl oxygens of the protein backbone represent the hydrophilic inter-action sites along one side of the otherwise hydrophobic AQP channel NPI; SPAR.

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The height of a residue symbol reflects the subfamily’s

degree of distinction at this site Ser186 turned out to

be the most characteristic residue for the Burkholderia

aquaglyceroporins (4.9 bit) Other prominent positions,

such as Asp190 (2.7 bit), denoted residues that are

gen-eral discriminators between orthodox AQPs and

aqua-glyceroporins [17]

The exchange of Asn for Ser in the NPA region

may have structural and functional consequences

Hence, we generated a structure model of the B

ceno-cepaciaaquaglyceroporin [B cenocepacia glycerol

facil-itator (BccGlpF)], by mapping the protein sequence on

the 2.2-A˚ resolution crystal structure of EcGlpF

(Pro-tein Data Bank: 1FX8) [13] (Fig 1B) Being shorter by

one methylene group, Ser186 enlarges the diameter in

the NPA region by about 20% of the average diameter

of the remaining channel, leaving the ar⁄ R region

around Arg189 as the only constriction in the channel

path Ser186 may form two stabilizing hydrogen bonds

between its hydroxyl oxygen and the backbone amide

nitrogens at the preceding two amino acid positions,

similar to the hydrogen bonds between the Asn64

car-bonyl oxygen and the backbone of the second

half-helix (green dotted lines in Fig 1B) The Asn64 side

chain amide also provides two hydrogen donor sites for

interaction with passing water and solute molecules,

whereas the Ser186 hydroxyl moiety acts as a donor for

a single hydrogen bond It is not clear whether this

hydrogen is accessible from within the channel, owing

to major differences in its position and orientation as

compared with the hydrogens of an Asn side chain

amide To address the question of whether the presence

of an SPA motif in BccGlpF affects channel

permeabil-ity or selectivpermeabil-ity, we cloned the respective ORF from

genomic DNA of B cenocepacia for site-directed

muta-genesis, expression, and functional analysis

Expression of wild-type BccGlpF and mutants

Like to other bacterial AQPs, BccGlpF was not

expressed in Xenopus laevis oocytes However, we

obtained good expression in the Saccharomyces

cerevi-siaeyeast system (Fig 2), which was used for the

fol-lowing functional analysis We generated several

BccGlpF mutants in which Asn64 was changed to Ala,

Asp, or Ser, and Ser186 was changed to Ala, Asn,

Asp, Cys, or Thr, and one double mutant with

switched positions of Asn and Ser, i.e N64S⁄ S186N

We chose as substitutes only small residues with side

chains smaller than or the same size as the Asn side

chain, because it has been shown in an early AQP

study that slightly larger residues, such as Gln, impair

channel function [18], and a major change to Lys was

found to suppress expression of AQP1 in humans, leading to a Colton-null phenotype [19]

Comparison of the BccGlpF mutant expression levels in yeast by semiquantitative densitometry of western blots showed three categories (Fig 2): (a) expression level similar to that of wild-type BccGlpF (N64A, N64S, N64S⁄ S186N, and S186N); (b) five-fold

to 10-fold reduced expression (N64D, S186C, and S186D); and (c) undetectable expression (S186A and S186T) Dimers of 54 kDa and higher-order complexes

of the expressed AQPs were visible when sufficient protein was loaded

Water and glycerol permeability of wild-type BccGlpF and mutants

To test for water permeability, we expressed wild-type BccGlpF and mutants in a yeast strain that lacked the endogenous aquaglyceroporin S cerevisiae glycerol facilitator [20], prepared yeast protoplasts, and sub-jected them to an outward-directed osmotic sorbitol gradient of 300 mosmÆkg)1 in a rapid mixing device The resulting cell shrinkage was determined by moni-toring the relative increase in light scattering (Fig 3A, left panel) Here, only the control cells expressing mammalian AQP1 [21] showed a rapid cell volume change caused by water efflux, which was 15-fold fas-ter than that of nonexpressing cells (Fig 3A, left panel and insert) Expression of wild-type BccGlpF or mutants did not increase the water flux above that of cells without AQP expression (Fig 3B, left panel) Similarly, the water permeability of EcGlpF was too low to be detected, which is consistent with earlier studies that have shown a one order of magnitude lower water permeability of EcGlpF than that of water-specific AQPs [22]

Fig 2 Relative expression levels of wild-type (wt) BccGlpF and mutants in yeast by western blot The proteins were detected via N-terminal HA-tags and a specific antiserum The bands at 54 kDa correspond to protein dimers Higher-order complexes can also be seen.

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Glycerol permeability was measured with the same

cells and an outward-directed osmotic glycerol gradient

of 300 mosmÆkg)1 Under these conditions, the

protop-lasts first shrunk because of water efflux Subsequently,

in a second phase, the volume recovered partially in

the presence of functional glycerol channels, owing to

glycerol influx following the chemical gradient

(Fig 3A, right panel) We chose this biphasic setup

because an isotonic glycerol gradient as typically used

with Xenopus oocytes [7] did not yield a robust assay

system EcGlpF served as a positive control, showing

the expected volume recovery effect (Fig 3A, right

panel and insert) BccGlpF exhibited the same degree

of glycerol permeability as EcGlpF (Fig 3B, right panel), confirming functionality of the novel Burk-holderia aquaglyceroporin Analysis of the BccGlpF mutants with any combination of Asn and Ser in both NPA motifs (N64S, S186N, and N64S⁄ S186N) showed equal glycerol permeability as obtained with the wild type, and Arrhenius activation energies of approxi-mately 6 kcalÆmol)1, whereas the remaining mutants (N64A, N64D, S186C, S186D, and S186T) were non-functional (Fig 3B, right panel)

Together, BccGlpF water and glycerol permeability are comparable to those seen with GlpF, and Asn and Ser are interchangeable in both BccGlpF NPA motifs without affecting glycerol permeability

Methylamine permeability of wild-type BccGlpF and mutants

To test for solute selectivity of the BccGlpF mutants,

we employed a sensitive phenotypic yeast assay for methylamine permeability [2] Methylamine is an ana-logue of ammonia and, similarly, its protonation status depends on the environmental pH (pKa= 10.6) For example, at pH 6.5, only 0.008% of the compound will

be in the unprotonated methylamine form, whereas 99.992% will be protonated as methylammonium Yeast cells endogenously express ammonium transport-ers of the S cerevisiae methylamine permease family, which transport protonated methylammonium into the cells independently of the external pH [23] As methy-lammonium is toxic to the yeast, the cells can only sur-vive when the compound is immediately shuttled out again Aquaglyceroporins have been shown to pass unprotonated methylamine if a pH gradient is gener-ated from an intracellular pH 6.8 to a more acidic external pH Accordingly, yeast expressing EcGlpF grows well on methylammonium-containing agar plates

at pH 5.5, whereas a flat pH gradient (pH 6.5) allows for only weak growth (Fig 4) Cells without an aqua-glyceroporin do not grow, owing to accumulation of toxic methylammonium Wild-type BccGlpF and the same set of mutants that conducted glycerol (N64S, S186N, and N64S⁄ S186N) rescued yeast growth, con-firming functionality of these channels (Fig 4) How-ever, we found that three more mutants that were impermeable for glycerol conducted the smaller methylamine, i.e BccGlpF N64A, S186C, and S186D Cell growth of yeast expressing the BccGlpF N64A mutant was as high as that of yeast with wild-type BccGlpF, whereas yeast expressing the BccGlpF S186C or S186D mutants grew considerably more slowly (Fig 4), correlating with the expression levels

A

B

Fig 3 Water and glycerol permeability of wild-type (wt) BccGlpF

and mutants (A) Changes in light scattering of yeast protoplasts in

a 300 m M osmotic sorbitol gradient for measuring water

permeabil-ity (left panel) or in a 300 m M osmotic glycerol gradient for glycerol

permeability (right panel) Nonexpressing cells (–) and cells

express-ing rat AQP1 (for water) or EcGlpf (for glycerol) were used as

con-trols The parts of the traces that are relevant for calculation of the

permeability coefficients are enlarged in the inserts (B)

Permeabil-ity coefficients for water (Pf) and glycerol (Pgly) For evaluation, six

to 10 traces from each of two independent experiments were

aver-aged The error bars denote standard error of the mean.

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determined by western blot (Fig 2) Again, the

remaining BccGlpF mutants (N64D, S186A, and

S186T) were nonfunctional

Water and ion permeability of a mammalian

AQP1 N76S mutant

Having established that Asnfi Ser exchanges in the

NPA motifs of BccGlpF do not alter glycerol and

methylamine permeability, we investigated whether

water permeability or ion exclusion might be affected

BccGlpF, however, could not be studied effectively in

the respective assays: the water permeability was too

low, and the protein was not made in Xenopus oocytes

As an alternative, we generated an analogous AQP1

N76S mutant that is well expressed in Xenopus

oocytes Also, ion permeability of AQPs has been found

and described only in selected mutants of AQP1, such as

AQP1 R195V [2,5] The AQP1 R195V mutant mimicks

the situation found in the group of AQPs that carry only

uncharged residues in the ar⁄ R pore constriction

Together, the AQP1 N76S single mutant and AQP1

N76S⁄ R195V double mutant allowed us to study the

effect of an SPA motif on water, proton, potassium and

sodium permeability, and to compare the results with

previously established data [2] (Fig 5)

The water permeability of the AQP1 N76S mutant

was identical to that of wild-type AQP1 and the AQP1

R195V mutant (Fig 5, upper left panel) and 20-fold

higher than that obtained with nonexpressing control

oocytes The AQP1 N76S⁄ R195V double mutant

showed a 32% reduction in water permeability, which

is similar in trend to a former AQP1 N76D⁄ H180A ⁄

R195V mutant, which exhibited an 86% reduction [5]

We then measured the ion conductance of wild-type AQP1 and the mutants in comparison with nonex-pressing control oocytes, using two-electrode voltage-clamp and a protocol described previously [2,5] For testing of proton conductance, an inward gradient was established by shifting the bath pH to 5.5 However, the currents obtained were not significantly different in control oocytes (not shown), wild-type AQP1-express-ing oocytes, and AQP1 N76S-expressing oocytes (Fig 5, upper right panel) This indicates that the AQP1 N76S mutant is impermeable for protons How-ever, we reproduced the proton leak of the AQP1 R195V mutant [2], which was further enhanced in the AQP1 N76S⁄ R195V double mutant by a factor of 3

Fig 4 Phenotypic yeast assay for methylamine permeability of

wild-type BccGlpF and mutants Cell growth at acidic pH indicates

efflux of toxic methylamine from the cells via the expressed

aqua-glyceroporins Nonexpressing cells (–) and cells expressing EcGlpF

were used as controls The control plate without addition of

methyl-amine demonstrates even loading of the samples.

Fig 5 Water, proton, potassium and sodium permeability of wild-type (wt) AQP1, and AQP1 ar ⁄ R or NPA mutants, in X laevis oocytes Water permeability (upper left panel) was calculated from oocyte shrinkage in medium supplemented with 20 m M mannitol Control oocytes without AQP1 expression (native) showed 20-fold lower water permeability For cation permeability, a two-electrode voltage clamp setup was used, with a voltage stepping protocol from +40 mV to )120 mV, and a 150-ms duration of each step The steady-state currents were recorded after 100 ms Respective cation gradients were generated by a pH shift in the bath from 7.4

to 5.5 (upper right panel; for proton permeability), replacement of

25 m M Ch in the bath by potassium (lower left panel), or replace-ment of 50 or 100 m M Ch for sodium (lower right panel) Cation permeability of control oocytes without AQP1 expression was not significantly different from that of oocytes expressing wild-type AQP1, and are not shown Error bars denote standard errors of the mean The asterisks indicate values that are significantly different from those obtained with wild-type AQP1.

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Permeability for alkali cations was measured by

par-tial, isotonic replacement of impermeable choline (Ch) in

the bathing solution with potassium or sodium, and

application of the voltage stepping protocol Significant

potassium currents above those of control oocytes were

not detectable in any of the tested AQP1 variants

How-ever, expression of the AQP1 N76S mutant robustly

increased the sodium current two-fold over control or

AQP1-expressing oocytes, and we even observed a

five-fold increase with the AQP1 N76S⁄ R195V mutant The

AQP1 R195V mutant was impermeable for sodium ions

In summary, our data show that Asnfi Ser

exchanges in the NPA motifs are well tolerated during

protein biosynthesis, and that the resulting AQP

chan-nels display normal water and solute permeability but

leak sodium ions

Discussion

Various statistical analyses of data from protein

struc-ture databases have ranked the 20 proteinogenic amino

acids according to their frequency at N-terminal helix

caps [24–27] Accordingly, mainly four residues are

strongly preferred at the Ncap position: Asn, Asp, Ser,

and Thr The following Ncap+1 position is typically

occupied by a Pro, whereas the degree of variation at

Ncap+2 increases drastically The findings are in

strik-ing agreement with the situation found at the

N-termi-nal ends of the characteristic AQP half-helices, which

carry canonical NPA motifs with an almost invariable

Asn position and somewhat less conserved Pro and Ala

positions [7–11] Averaged over the full set of proteins

in the database, a helix cap position does not display a

preference among Asn, Asp, Ser, or Thr However, in

the subset of AQP half-helices, 99% of the Ncap

posi-tions are filled with an Asn, and the remaining 1% is

shared between Ser and probably Cys, with the Cys

being predicted but not yet experimentally confirmed

What is the reason for this strong preference for

Asn? Considering the spatial restrictions in the centre

of the AQP channel, it seems evident that only residues

smaller than or of the same size as Asn are tolerated in

the half-helix Ncap position Indeed, larger residues at

these sites have been shown to block the AQP1 channel

or even to massively interfere with AQP1 expression

[18,19] Despite its small size, Thr appeared to fully

abolish expression of the respective AQP mutant This

phenomenon may be explained by the b-branched

molecular structure of Thr, which can interfere with

protein function [28,29] The branching next to the

car-bon atom carrying the amino group may clash with the

dense packing in the NPA protein region Putting an

Ala at the Ncap position produced ambiguous results

Replacement of Asn by Ala at the first NPA site was fully compatible with protein expression, and even pro-duced to a functional channel with methylamine perme-ability However, the permeability profile was altered because glycerol was no longer conducted This may hint at influences on the channel structure, probably owing to the lack of stabilizing hydrogen bonds between the Ncap residue – Ala is neither donor nor acceptor – and the half-helix backbone Higher flexibil-ity in this region may prevent the larger glycerol from passing, whereas methylamine is still compatible with the slightly changed situation The effect of S186C and S186D may be similarly explained Ala at the Ncap posi-tion of the second NPA motif (SPA in BccGlpF) was not tolerated, yielding no protein Hence, the second NPA site appears to be structurally more critical than the first NPA site This may be related to the immedi-ately following Arg as a major constituent of the criti-cal selectivity filter at the ar⁄ R constriction (Fig 1B)

In contrast to replacement by Ala and Thr, replace-ment of Asn by Ser in either NPA motif produced a fully functional AQP However, Ser is a rare residue at the AQP half-helix caps Our finding of a sodium leak

in the AQP1 N76S mutant provides an argument for the strong preference for Asn Steady sodium leak cur-rents across the cell membrane require active export of sodium from the cytosol by ATPases, in order to maintain the cell’s resting potential, and thus interfere with bioenergetics [30] Even a small additional leak enhances the energetic costs of the cell, and therefore represents an evolutionary disadvantage We have shown previously that replacement of Asn in the NPA motifs by Asp generates a sodium leak, which is four-fold larger than that with Ser [5] Asp and Ser carry oxygen atoms in their side chains as putative coordina-tion sites for sodium ions, and so may interfere with the electrostatic barrier function of the half-helix dipoles by increasing the probability of the presence of

a sodium ion in the channel centre It is tempting to analyse natural AQPs with predicted DPA as well as CPY motifs [11] with regard to cation exclusion Together, Asn residues appear to be optimal in the N-capping NPA motifs of the AQP half-helices with regard to protein stability and cation exclusion, but not in terms of solute selectivity

Experimental procedures

Cloning and site-directed mutagenesis of BccGlpF

The ORF of the BccGlpF-encoding gene was amplified

by PCR from genomic B cenocepacia DNA (German

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Collection of Microorganisms and Cell Cultures, DSMZ)

and cloned into the yeast expression plasmid pDR196 An

N-terminal haemagglutinin (HA) epitope tag was inserted

via a synthetic SpeI–HA–PstI oligonucleotide dimer into

respective sites of the plasmid Point mutations were

intro-duced with the QuikChange protocol (Stratagene,

Heidel-berg, Germany) and primers with respective nucleotide

exchanges Correct amplification and mutagenesis were

confirmed by DNA sequencing A primer list is available

from the authors upon request

Expression of BccGlpF in S cerevisiae and

membrane preparation for western blot

BY4742Dfps1 (MATa his3D1 leu2D0 ura3D0

fps1::Kan-MX4) yeast cells (Euroscarf, Frankfurt, Germany) were

transformed with the generated pDR196–BccGlpF

con-structs Single colonies were picked and grown overnight in

washed with ice-cold water and extraction buffer (5 mm

EDTA, 25 mm Tris, pH 7.5) plus protease inhibitor

cock-tail (Roche, Mannheim, Germany), resuspended in

extrac-tion buffer, and vortexed with acid-washed glass beads The

and the membranes were collected from the supernatants

determined by use of the Bradford method, with BSA as a

standard For semiquantitative densitometric analysis of the

expression levels in yeast, equal amounts of total protein

the lanes by Coomassie Blue staining, blotted onto

poly(vinylidene difluoride) membranes, and detected with a

monoclonal mouse antibody against the N-terminal HA

epitope tags (Roche)

Measurement of water and glycerol permeability

by stopped-flow assay

Yeast protoplasts were prepared from cells expressing

wild-type BccGlpF, BccGlpF mutants, EcGlpF or AQP1 by

digesting the cell wall with zymolyase-20T according to Bertl

mea-surement of water permeability, the suspension was rapidly

mixed with an equal volume of osmotic buffer (incubation

buffer supplemented with 0.6 m sorbitol) in a stopped-flow

apparatus (SFM-300; BioLogic, Claix, France) Cell volume

changes were monitored by measuring the intensity of 90

light scattering at 546 nm The osmotic water permeability

coefficient Pf was calculated from Pf= 1⁄ sV0⁄ (S0VWCdiff)

[31], where s is the time constant of the exponential fitting

the partial molar water volume (18 cm3Æmol)1), and Cdiffthe concentration of the osmotically active solute after mixing

measured by mixing with glycerol buffer (incubation buffer supplemented with 0.6 m glycerol) The glycerol permeability

light scattering curve, using Pgly= |dI⁄ dt|(V0Cout)⁄ (S0Cdiff), where dI⁄ dt is the slope of the intensity curve, V0and S0are

(1.5 m), and Cdiffis the chemical glycerol gradient (0.3 m) In each experiment, six to 10 trace curves were recorded and

for calculation of the Arrhenius activation energy

Phenotypic S cerevisiae methylamine efflux assay

The assay was performed as described previously [2] In

BccGlpF and mutants, or EcGlpF, were grown overnight

cultures were harvested by centrifugation (16 000 g, 30 s),

1 : 10 dilutions on SD agar medium supplemented with 3% glucose, 0.1% proline as the sole nitrogen source, and

50 mm methylamine at pH 5.5 and 6.5 Cell growth was monitored after 5 days

Expression of rat wild-type AQP1 and mutants in

X laevis oocytes and water permeability

Rat AQP1 and the AQP1 R195V mutant in the pOG1 vec-tor have been described previously [2] The N76S point mutation was introduced with the QuikChange protocol (Stratagene) cRNA synthesis was performed with NotI lin-earized pOG1 plasmid with the mMessage mMachine T7 kit (Ambion, Darmstadt, Germany) Five nanograms of cRNA in 50 nL of water was injected into collagenase A (Roche)-defolliculated stage V and VI X laevis oocytes

within 10 s after addition of 20 mm mannitol to the bathing solution from the rate of oocyte shrinkage [2]

Electrophysiology

To measure cation-induced currents in Xenopus oocytes, we used the two-electrode voltage-clamp technique as described previously [2,5] In short, microelectrodes were inserted into oocytes superfused with control solution (100 mm ChCl,

10 mm Hepes or Mes, pH 7.4) or with test solutions at a

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rate of 20 mLÆmin)1 To measure the H+permeability, the

and after the solution change, the voltage of the

voltage-clamped oocyte was jumped to potentials between +40 and

)140 mV in steps of 20 mV lasting 150 ms Corresponding

steady-state clamp currents were recorded after 100 ms

Acknowledgements

We thank B Henke and C Steinbronn for technical

assistance This work was supported by the Deutsche

Forschungsgemeinschaft Be2253⁄ 3 (to E Beitz) and

grants from the Danish Research Council, the

Lund-beck Foundation, and Loevens (to T Zeuthen)

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Supporting information

The following supplementary material is available: Fig S1 Alignment of Burkholderia aquaglyceroporins

in comparison with Escherichia coli glycerol facilitator (EcGlpF)

This supplementary material can be found in the online version of this article

Please note: As a service to our authors and readers, this journal provides supporting information supplied

by the authors Such materials are peer-reviewed and may be re-organized for online delivery, but are not copy-edited or typeset Technical support issues arising from supporting information (other than missing files) should be addressed to the authors

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