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The view that parasites can develop cooperative symbiotic relationships with their hosts is both appealing and widely held; however, there is no molecular genetic evidence of such a transition. Here we demonstrate that a mutualistic bacterial endosymbiont of grain weevils maintains and expresses inv/spa genes encoding a type III secretion system homologous to that used for invasion by bacterial pathogens. Phylogenetic analyses indicate that inv/spa genes were present in presymbiotic ancestors of the weevil endosymbionts, occurring at least 50 million years ago. The function of inv/spa genes in maintaining symbiosis is demonstrated by the up-regulation of their expression under both in vivo and in vitro conditions that coincide with host cell invasion.

Because of its possible importance in cystic fibrosis (CF) pulmonary pathogenesis, the effect of anion and liquid secretion inhibitors on airway mucociliary transport was examined. When excised porcine tracheas were treated with ACh to induce gland liquid secretion, the rate of mucociliary transport was increased nearly threefold from 2.5 [+ or -] 0.5 to 6.8 [+ or -] 0.8 mm/min. Pretreatment with both bumetanide and dimethylamiloride (DMA), to respectively inhibit [Cl.sup.-] and HC[O.sup.-.sub.3] secretion, significantly reduced mucociliary transport in the presence of ACh by 92%. Pretreatment with the anion channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid similarly reduced mucociliary transport in ACh-treated airways by 97%. These agents did not, however, reduce ciliary beat frequency. Luminal application of benzamil to block liquid absorption significantly attenuated the inhibitory effects of bumetanide and DMA on mucociliary transport. We conclude that anion and liquid secretion is essential for normal mucociliary transport in glandular airways. Because the CF transmembrane conductance regulator protein likely mediates [Cl.sup.-], HC[O.sup.-.sub.3], and liquid secretion in normal glands, we speculate that impairment of gland liquid secretion significantly contributes to defective mucociliary transport in CF. cystic fibrosis; submucosal glands; chloride secretion; ciliary beat frequency; bicarbonate secretion

Cleavage of proline-264 of YscU protein in the Yersinia type III secretion system does not affect Yop secretion but is required for maintaining a nontoxic fold for the bacterium survival.

The type III secretion system, mxiE, functions as a transcription regulator and regulates six virulence plasmid-encoded genes, which are activated by MxiE within the cellular environment of Shigella flexneri following its host cell invasion.

Research has been conducted on the gram-negative Shigella bacterium's type III secretion system. The generation of spa32 mutant and localization of the Spa32 protein in this bacterium have been carried out in investigating the genes required for Ipa protein secretion and the results are reported.

A novel secretion pathway originally found in plants has recently been discovered in bacteria and termed TAT, for 'twin-arginine translocation,' with respect to the presence of an Arg-Arg motif in the signal sequence of TAT-secreted products. However, it is unknown whether the TAT system contributes in any way to virulence through the secretion of factors associated with pathogenesis or stress response. We found that the opportunistic pathogen Pseudomonas aeruginosa produces several virulence factors that depend on the TAT system for proper export to the periplasm, outer membrane, or extracellular milieu. We identified at least 18 TAT substrates of P. aeruginosa and characterized the pleiotropic phenotypes of a tatC deletion mutant. The TAT system proved essential for the export of phospholipases, proteins involved in pyoverdine-mediated iron-uptake, anaerobic respiration, osmotic stress defense, motility, and biofilm formation. Because all these traits have been associated with virulence, we studied the role of TAT in a rat lung model. A tatC mutant did not cause the typical multifocal pulmonary abscesses and did not evoke a heavy inflammatory host response compared with wild type, indicating that tatC mutant cells are attenuated for virulence. Because the TAT apparatus is well conserved among important bacterial pathogens yet absent in mammalian cells, it represents a potential target for novel antimicrobial compounds.

SEC2 is an essential gene required for polarized growth of the yeast Saccharomyces cerevisiae. It encodes a protein of 759 amino acids that functions as a guanine nucleotide exchange factor for the small GTPase Sec4p, a regulator of Golgi to plasma membrane transport. Activation of Sec4p by Sec2p is needed for polarized transport of vesicles to exocytic sites. Temperature-sensitive (ts) mutations in sec2 and sec4 result in a tight block in secretion and the accumulation of secretory vesicles randomly distributed in the cell. The proper localization of Sec2p to secretory vesicles is essential for its function and is largely independent of Sec4p. Although the ts mutation sec2-78 does not affect nucleotide exchange activity, the protein is mislocalized. Here we present evidence that Ypt31/32p, members of Rab family of GTPases, regulate Sec2p function. First, YPT31/YPT32 suppress the sec2-78 mutation. Second, overexpression of Ypt31/32p restores localization of Sec2-78p. Third, Ypt32p and Sec2p interact biochemically, but Sec2p has no exchange activity on Ypt32p. We propose that Ypt32p and Sec4p act as part of a signaling cascade in which Ypt32p recruits Sec2p to secretory vesicles; once on the vesicle, Sec2p activates Sec4p, enabling the polarized transport of vesicles to the plasma membrane.

The yopQ protein secretion signal in Yersinia enterocolitica is controlled by yopQ codons in that codons 1 to 10, 1 to 11, and 1 to 12 abolish secretion, whereas codons 1 to 13, 1 to 14, and 1 to 15 do not. Further, the translation of the yopQ secretion signal is necessary for the type III transport of YopQ.

Results demonstrate that both TldD and TldE proteins mediate microcin B17 secretion in Escherichia coli and in the mutants lacking the cognate genes, micromicin B17 accumulates without being exported. Further, the proteins affect CcdA and CcdA41 antidote stability.

The influence of the master regulatory operon of the flagellum, flhDC, on the yop regulon in Yersinia enterocolitica is evaluated. Data show that in a mutant, the yop regulon is up-regulated and temperature independent, suggesting that in wild-type bacteria, flhDC represses the yop regulon.

Cerebral osmoreceptors mediate thirst and neurohypophyseal secretion stimulated by increases in the effective osmolality of plasma ([P.sub.osmol]). The present experiments determined whether an intragastric load of hypertonic saline (ig HS; 0.5 M NaCl, 4 ml) would potentiate these responses before induced increases in [P.sub.osmol] in the general circulation could be detected by cerebral osmoreceptors. Adult rats deprived of water overnight and then given intragastric HS consumed much more water in 15-30 min than rats given either pretreatment alone, even though systemic [P.sub.osmol] had not yet increased significantly because of the gastric load. In other rats pretreated with an intravenous infusion of 1 M NaCl (2 ml/h for 2 h), plasma levels of vasopressin and oxytocin were considerably elevated 15 and 25 min after intragastric HS treatment, whereas systemic [P.sub.osmol] was not increased further. These and other findings are consistent with previous reports that hepatic portal osmoreceptors (or [Na.sup.+] receptors) stimulate thirst and neurohypophyseal hormone secretion in euhydrated rats given gastric NaCl loads and indicate that these effects are potentiated when animals are dehydrated. osmoreceptors; oxytocin; vasopressin; water intake

To define developmental changes in atrial natriuretic peptide (ANP) secretion and in the cross talk between C-type natriuretic peptide (CNP) and ANP, we performed experiments in isolated perfused nonbeating cardiac atria isolated from rabbits between 1 and 8 wk of age. Changes in atrial pressure resulted in increases in atrial volume that rose with age and reached the peak value at 4 wk. A rise in volume change increased ANP secretion with concomitant translocation of extracellular fluid (ECF) into the atrial lumen, which increased with age and reached the peak value at 4 wk. The positive relationship between stretch-induced ANP secretion and ECF translocation shifted upward and leftward with age. CNP suppressed stretch-induced ANP secretion in the 8-wk-old group but not in the 2- and 4-wk-old groups without differences in ECF translocation and atrial volume. Therefore, the ANP secretion in terms of ECF translocation was markedly suppressed by CNP in the 8-wk-old group but not in the 2- and 4-wk-old groups. The production of cGMP by CNP in atrial tissue membranes was markedly attenuated in young rabbits. However, 8-bromo-cGMP suppressed stretch-induced ANP secretion in 2- and 8-wk-old groups. Natriuretic peptide receptor-B mRNA was similar in both groups. Therefore, we conclude that the inhibitory effect of CNP on atrial ANP secretion is developmentally regulated, being absent during normal cardiac development in young animals and intact in adult animals. guanylyl cyclase-B; development; extracellular fluid translocation; stretch

Pancreatic islets contain ionotropic glutamate receptors that can modulate hormone secretion. The purpose of this study was to determine whether islets express functional group III metabotropic glutamate (mGlu) receptors. RT-PCR analysis showed that rat islets express the mGlu8 receptor subtype. mGlu8 receptor immunoreactivity was primarily displayed by glucagon-secreting [alpha]-cells and intrapancreatic neurons. By demonstrating the immunoreactivities of both glutamate and the vesicular glutamate transporter 2 (VGLUT2) in these cells, we established that [alpha]-cells express a glutamatergic phenotype. VGLUT2 was concentrated in the secretory granules of islet cells, suggesting that glutamate might play a role in the regulation of glucagon processing. The expression of mGlu8 by glutamatergic cells also suggests that mGlu8 may function as an autoreceptor to regulate glutamate release. Pancreatic group III mGlu receptors are functional because mGlu8 receptor agonists inhibited glucagon release and forskolin-induced accumulation of cAMP in isolated islets, and (R,S)-cyclopropyl-4-phosphonophenylglycine, a group III mGlu receptor antagonist, reduced these effects. Because excess glucagon secretion causes postprandial hyperglycemia in patients with type 2 diabetes, group III mGlu receptor agonists could be of value in the treatment of these patients. glutamate; glucagon; vesicular glutamate transporter 2; (R,S)-4-phosphonophenylglycine; (S)-3,4-dicarboxyphenylglycine; (R,S)-cyclopropyl-4-phosphonophenylglycine; cyclic adenosine monophosphate

Research has been conducted on the atypical secM signal peptide. The characterization of this peptide has been carried out and the results demonstrate that the peptide's amino-terminal and hydrophobic core regions have different functions.

In eukaryotic cells, secretion is achieved by vesicular transport. Fusion of such vesicles with the correct target compartment relies on SNARE proteins on both vesicle (v-SNARE) and the target membranes (t-SNARE). At present it is not clear how v-SNAREs are incorporated into transport vesicles. Here, we show that binding of ADP-ribosylation factor (ARF)--GTPase-activating protein (GAP) to ER-Golgi v-SNAREs is an essential step for recruitment of Arf1p and coatomer, proteins that together form the COPI coat. ARF-GAP acts catalytically to recruit COPI components. Inclusion of v-SNAREs into COPI vesicles could be mediated by direct interaction with the coat. The mechanisms by which v-SNAREs interact with COPI and COPII coat proteins seem to be different and may play a key role in determining specificity in vesicle budding.

During the SecB stimulation of SecA ATPase activity, SecB interacts with SecA inducing a conformational change that favors ATP binding and hydrolysis. Data show that SecB-enhanced Seca ATPase activity is due to an increase in the ATP hydrolysis rate. Further, the conformation of the high-affinity nucleotide binding site is regulated by SecB.

Results reveal that the TonB-facilitated proton-motive-force does not regulate the type 4 pilus biogenesis and type II secretion in Vibrio cholerae as shown by the mutants defective for TonB.

Results reveal that the extracellular proteins of Vibrio cholerae exhibit an extracellular transport signal of the endochitinase, which is localized to a region between amino acids 75 and 555 of the enzyme. Data indicate that the transport signal protein is a structural motiff of the enzyme endochitinase.

Research has been conducted on the expression type III secretion substrate regulation. The effect of the activated by the environmental calcium signal type III pathway on the YopQ synthesis has been investigated and the characterization of the mutants permitting this synthesis has been carried out and is described.

The molecular mechanisms underlying early/recycling endosomes-to-TGN transport are still not understood. We identified interactions between the TGN-localized putative t-SNAREs syntaxin 6, syntaxin 16, and Vti1a, and two early/recycling endosomal v-SNAREs, VAMP3/cellubrevin, and VAMP4. Using a novel permeabilized cell system, these proteins were functionally implicated in the post-Golgi retrograde transport step. The function of Rab6a' was also required, whereas its closely related isoform, Rab6a, has previously been implicated in Golgi-to-endoplasmic reticulum transport. Thus, our study shows that membrane exchange between the early endocytic and the biosynthetic/ secretory pathways involves specific components of the Rab and SNARE machinery, and suggests that retrograde transport between early/recycling endosomes and the endoplasmic reticulum is critically dependent on the sequential action of two members of the Rab6 subfamily.

Activation of ion secretion via proteinase-activated receptor-2 in human colon. Am J Physiol Gastrointest Liver Physiol 282: G200-G210, 2002. First published September 21, 2001; 10.1152/ajpgi.00137.2001. Proteinase-activated receptor (PAR) type 2 (PAR-2) has been shown to mediate ion secretion in cultured epithelial cells and rat jejunum. With the use of a microUssing chamber, we demonstrate the role of PAR-2 for ion transport in native human colonic mucosa obtained from 30 normal individuals and 11 cystic fibrosis (CF) patients. Trypsin induced [Cl.sup.-] secretion when added to the basolateral but not luminal side of normal epithelia. Activation of [Cl.sup.-] secretion by trypsin was inhibited by indomethacin and was further increased by cAMP in normal tissues but was not present in CF colon, indicating the requirement of luminal CF transmembrane conductance regulator. Effects of trypsin were largely reduced by low [Cl.sup.-], by basolateral bumetanide, and in the presence of barium or clotrimazole, but not by tetrodotoxin. Furthermore, trypsin-induced secretion was inhibited by the [Ca.sup.2+]-ATPase inhibitor cyclopiazonic acid and in low-[Ca.sup.2+] buffer. The effects of trypsin were almost abolished by trypsin inhibitor. Thrombin, an activator of PAR types 1, 3, and 4, had no effects on equivalent short-circuit currents. The presence of PAR-2 in human colon epithelium was confirmed by RT-PCR and additional experiments with PAR-2-activating peptide. PAR-2-mediated intestinal electrolyte secretion by release of mast cell tryptase and potentiation of PAR-2 expression by tumor necrosis factor-[alpha] may contribute to the hypersecretion observed in inflammatory processes such as chronic inflammatory bowel disease. protease-activated receptors; ion transport; trypsin; cystic fibrosis transmembrane conductance regulator; inflammatory bowel disease

This article discusses the architectural, topofunctional, and molecular aspects of N-linked oligosaccharide biosynthesis in the endoplasm reticulum and the golgi apparatus. The quality aspects of the glycosylated proteins along with the role of golgi apparatus and oligosaccharide structures to cell surface glycoproteins are reviewed.

Results demonstrate that GacA protein upregulates the expression of regulatory RNA, RsmZ, in Pseudomonas fluorescens CHA0 in response to a bacterial signal. This leads RsmZ to alleviate the respression activity of RsmA on target mRNAs expression.

Results demonstrate that the expression of signal peptidases is enhanced in the absence of ClpXP protease leading to an increased level of secretion defective ATP-binding cassette (ABC) transporter (ecs) mutants. Data indicate that the mechanism of signal peptide cleavage of secretory proteins by ClpXP and Ecs is different.

Purified native form of secretogranin II, from bovine adrenal medullary chromaffin cell secretory granules, predominantly exhibits beta-sheet and random coil structures with low level of alpha-helicity. Data indicate that it undergoes a pH-dependent conformational change, acidic pH-, and calcium-dependent aggregation. Furthermore, secretogranin II participates in the biogenesis of secretory granules.

The adrenal gland is important for homeostatic responses to metabolic stress: hypoglycemia stimulates the splanchnic nerve, epinephrine is released from adrenomedullary chromaffin cells, and compensatory glucogenesis ensues. Acetylcholine is the primary neurotransmitter mediating catecholamine secretion from the adrenal medulla. Accumulating evidence suggests that a secretin-related neuropeptide also may function as a transmitter at the adrenomedullary synapse. Costaining with highly specific antibodies against the secretin-related neuropeptide pituitary adenylate cyclase-activating peptide (PACAP) and the vesicular acetylcholine transporter (VAChT) revealed that PACAP is found in nerve terminals at all mouse adrenomedullary cholinergic synapses. Mice with a targeted deletion of the PACAP gene had otherwise normal cholinergic innervation and morphology of the adrenal medulla, normal adrenal catecholamine and blood glucose levels, and an intact initial catecholamine secretory response to insulin-induced hypoglycemia. However, insulin-induced hypoglycemia was more profound and longer-lasting in PACAP knock-outs, and was associated with a dose-related lethality absent in wild-type mice. Failure of PACAP-deficient mice to adequately counterregulate plasma glucose levels could be accounted for by impaired long-term secretion of epinephrine, secondary to a lack of induction of tyrosine hydroxylase, normally occurring after insulin hypoglycemia in wild-type mice, and a consequent depletion of adrenomedullary epinephrine stores. Thus, PACAP is needed to couple epinephrine biosynthesis to secretion during metabolic stress. PACAP appears to function as an 'emergency response' cotransmitter in the sympathoadrenal axis, where the primary secretory response is controlled by a classical neurotransmitter but sustained under paraphysiological conditions by a neuropeptide.

Research shows that iron acquisition by Candida albicans is mediated by ferric reductase, p-phenylenediamine oxidase and ferrous transport and requires copper for the latter two functions. The global regulator TUP1 participates in the iron-dependent gene regulation.

This review unfolds the story of the unfolded protein response (UPR) process encountered with surface and secreted proteins in yeast and mammalian systems. The UPR begins when protein maturation, which involves protein folding, is interrupted at the endoplasm reticulum. Data indicate that three gene products can initiate the UPR in yeast and mammals.

Procollagen (PC)-I aggregates transit through the Golgi complex without leaving the lumen of Golgi cisternae. Based on this evidence, we have proposed that PC-I is transported across the Golgi stacks by the cisternal maturation process. However, most secretory cargoes are small, freely diffusing proteins, thus raising the issue whether they move by a transport mechanism different than that used by PC-I. To address this question we have developed procedures to compare the transport of a small protein, the G protein of the vesicular stomatitis virus (VSVG), with that of the much larger PC-I aggregates in the same cell. Transport was followed using a combination of video and EM, providing high resolution in time and space. Our results reveal that PC-I aggregates and VSVG move synchronously through the Golgi at indistinguishable rapid rates. Additionally, not only PC-I aggregates (as confirmed by ultrarapid cryofixation), but also VSVG, can traverse the stack without leaving the cisternal lumen and without entering Golgi vesicles in functionally relevant amounts. Our findings indicate that a common mechanism independent of anterograde dissociative carriers is responsible for the traffic of small and large secretory cargo across the Golgi stack.

The authors review publications on the Hedgehog family of intercellular signaling proteins. The topics of interest include mediated by Hedgehog local interactions in the embryonic ectoderm of Drosophila, long-range signaling in Drosophila imaging discs, Hedgehog reception and control of Hh secretion and distribution.

Research reveals that expression of the chiC gene, which encodes an extracellular chitinase in Pseudomonas aeruginosa, is regulated by the quorum sensing system. Results indicate that only a small amount is secreted after an overnight growth peroid, but after several days of growth, the enzyme is found in the culture medium.

In shigella base element pairs of ring-proteins MxiM-MxiD and MxiJ-mxiD of the cell envelope form a transmembrane structure, which mediates the assembly of needle complex of the type III secretion pathway. The base element MixM interacts with the major outer-membrane-associated ring-protein MxiD with the former affecting later's stability and structure.

Protein export function is mediated by two homologues of SecA, SecA1 and SecA2, in the Sec pathway of Mycobacteria. Results reveal that while SecA1 is essential, SecA2 assists SecA1 in the export of some proteins. Data indicate that both secA genes are conserved throughout Mycobacteria.

This review summarizes new research trends in the analysis and understanding of functional genomics of gram-positive bacteria. The microarrays technique and its application in identifying transcriptional regulatory proteins and defining transcriptomes is discussed.

Results show that the reduced cytolytic activity of the secreted alpha-hemolysin toxin by tolC mutants is due to the aggregation or misfolding of the toxin molecule. Data indicate that six of the mutations are localized to the alpha-helical domain of TolC, while two are embedded in the beta-barrel domain of TolC.

Shalamanova, Liliana, Bernd Kfibler, Jens-Gerd Scharf, and Thomas Braulke. MDCK cells secrete neutral proteases cleaving insulin-like growth factor-binding protein-2 to -6. Am J Physiol Endocrinol Metab 281: E 1221-E 1229, 2001.--Proteolysis of insulin-like growth factor-binding proteins (IGFBPs) may be an important mechanism to regulate IGF availability and IGF-independent functions of IGFBPs. We analyzed the secretion of IGFBP proteases in Madin-Darby canine kidney (MDCK) cells. The results showed that several specific proteases were secreted, cleaving IGFBP-2 to -6 at neutral pH. The proteolytic activity against IGFBP-6 differed at least from IGFBP-5 protease activity in its sensitivity both to IGF-II and to the hydroxamic acid-based disintegrin metalloprotease inhibitor, as well as serine protease inhibitors. During partial purification steps, the serine protease inhibitor-sensitive fraction with IGFBP-6 protease activity was separated from fractions characterized by the presence of a 30-kDa disintegrin immunoreactive band. Whereas the IGFBP-4 and -6 proteases are predominantly secreted across the basolateral membrane, the majority of IGFBPs are sorted to the apical mediun~ from filter-grown cells. These studies indicate that the side-specific secretion of several distinct IGFBP proteases with partially overlapping IGFBP specificities may be another level in the regulation of IGF-dependent epithelial functions. insulin-like growth factor-binding proteins and proteases; polarized sorting; disintegrin metalloprotease Received 15 November 2000; accepted in final form 16 July 2001

Sanders, Jennifer L., Naibedya Chattopadhyay, Olga Kifor, Toru Yamaguchi, and Edward M. Brown. [Ca.sup.2+]-sensing receptor expression and PTHrP secretion in PC-3 human prostate cancer cells. Am J Physiol Endocrinol Metab 281: E1267--E1274, 2001.--Prostate cancer metasta-sizes frequently to bone. Elevated extracellular calcium concentrations ([Ca.sup.2+][0.sub]) stimulate parathyroid hormone-related protein (PTHrP) secretion from normal and malignant cells, potentially acting via the [Ca.sup.2+][0.sub]-sensing receptor (CaR). Because prostate cancers produce PTHrP, if high [Ca.sup.2+][0.sub] stimulates PTHrP secretion via the CaR, this could initiate a mechanism whereby osteolysis caused by bony metastases of prostate cancer promotes further bone resorption. We investigated whether the prostate cancer cell lines LnCaP and PC-3 express the CaR and whether polycationic CaR agonists stimulate PTHrP release. Both PC-3 and LnCaP prostate cancer cell lines expressed bona fide CaR transcripts by Northern analysis and RT-PCR and CaR protein by immuno-cytochemistry and Western analysis. The polycationic CaR agonists [Ca.sup.2+][0.sub], neomycin, and spermine each concentration dependently stimulated PTHrP secretion from PC-3 cells, as measured by immuno-radiometric assay, with maximal, 3.2-, 3.6-, and 4.2-fold increases, respectively. In addition, adenovirus-mediated infection of PC-3 cells with a dominant negative CaR construct attenuated high [Ca.sup.2+][0.sub]-evoked PTHrP secretion, further supporting the CaR's mediatory role in this process. Finally, pretreating PC-3 cells with transforming growth factor (TGF)-[[beta].sub.1] augmented both basal and high [Ca.sup.2+][0.sub]-stimulated PTHrP secretion. Thus, in PTHrP-secreting prostate cancers metastatic to bone, the CaR could initiate a vicious cycle, whereby PTHrP-induced bone resorption releases [Ca.sup.2+][0.sub] and TGF-[beta] stored within bone, further increasing PTHrP release and osteolysis. parathyroid hormone-related protein; ion-sensing receptor; osteolysis; prostate cancer; LnCaP cells; skeletal metastases Received 26 September 2000; accepted in final form 11 July 2001

Results show that in Strptomyces lividans secretome exhibits the twin-arginine translocation pathway composed of one tatC, two hcf106 homologs, and several precursor proteins containing a twin-arginine motif. Data indicate that this pathway translates folded proteins.

Research shows that a two-step mechanism involving an onset processing and releasing of the immature secretory granules mediates the production of processing-competent organelles from the trans-Golgi apparatus.

Research has been conducted on the Yersinia enterocolitica which exports Yop protein via type III secretion pathway during infection. The suggestion that YopN transport may act as a regulation mechanism of the type III pathway is discussed.

Research shows that chromogranin A is a key regulator of dense-core secretory granule biogenesis as well as storage of other granule proteins in neuroendocrine cells. Data reveal that down regulation of chromogranin A results in the loss of dense-core secretory granules, hormone secretion, and reducion of secretory granule proteins.

Results reveal that the outer-membrane lipoprotein BfpB, involved in type IV bundle-forming pili formation, is a multimeric complex whose production and stability are dependent on its interaction with BfpG. Data indicate that BfpB mediates enteropathogenic Escherechia coli protein accumulation in the growth medium.

Research discusses the role of virE1 gene and its encoded product VirE1 secretion chaperone in mediating multifunctional effector protein VirE2 export via type IV secretion system in Agrobacterium tumefaciens. Data indicate that virE1 regulates virE2 translation, VirE1 protein stabilizes VirE2, and VirE1 forms a VirE1-VirE2 complex.

Results demonstrate the dependency of alpha-amylase secretion and proper protein folding on the cellular concentration of the lipoprotein PrsA in Bacillus subtilis. Data further sugest that PrsA is required for cell viability and its depletion leads to altered cellular morphology and cell death.

Results show that the type 1 secretion system component LipB is controlled by the swr quorum-sensing system in Serratia liquefaciens MG1. Data indicate that Lip exporter type 1 secretion system mediates extracellular lipase, metalloprotease, and S-layer protein.

Secretion of hybrid proteins carrying C-terminal fragments of Erwinia chrysanthemi protease B reveals that only proteins with the longer C terminus can promote the secretion. Data indicate that glycine-rich motifs carrying no disulfide bonds carry out an efficient secretion of the hybrid proteins.

Results show that the Klebsiella oxytoca cells defective in secretion of pullulanase, because of a mutation in the gene encoding a periplasmic disulfide oxidoreductase pullulanase, are rectified by the overproduction of pseudopilin PulK. Data indicate that pseudopilin contains reduced disulfide bonds, which impair the secretion process.

A genetic analysis of the pathogenicity island that forms the supramolecular structure, needle complex asembly, in Salmonella enterica serovar Typhimurium type 111 is presented. Results demonstrate that the assembly proceeds in discrete, genetically separable steps, which involve a sec-dependent step and a sec-independent process.

Results demonstrate that the active-site CXXC motifs of the dipeptide DsbA and DsbC are involved in the folding of the soluble Dsb thiol-disulfide oxidoreductases indepedently of the dipeptide's redox potential. The modulation of active sites enhance the disulfide isomerization and influence protein folding and secretion into the periplasmic space.

Results show that secretion specificity of exoproteins in Pseudomonas aeruginosa and P. alcaligenes is determined by XcpP and/or XcpQ homologs. However, data reveal that the homologs can not interchange with their counterparts between these two bacterial species, which requires a species-specific interactions between XcpP and XcpQ and another uncharacterized component.