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1.
Nicole Benhamou Pierre J. Lafontaine Dominique Mazau Marie-Thérèse Esquerré-Tugayé 《Planta》1991,184(4):457-467
An antiserum raised against deglycosylated hydroxyproline-rich glycoproteins (HPGPs) from melon (Cucumis melo L.) was used to study the relationship between Rhizobium infection and induction of HRGPs in bean (Phaseolus vulgaris L.) root nodule cells infected with either the wild-type or a C4-dicarboxylic acid mutant strain of Rhizobium leguminosarum bv. phaseoli. In effective nodules, where fixation of atmospheric dinitrogen is taking place, HRGPs were found to accumulate mainly in the walls of infected cells and in peribacteroid membranes surrounding groups of bacteroids. Internal ramifications of the peribacteroid membrane were also enriched in HRGPs whereas the peribacteroid space as well as the bacteroids themselves were free of these glycoproteins. In mutant-induced root nodules, HRGPs were specifically associated with the electron-dense, laminated structures formed in plastids as a reaction to infection by this mutant. The presence of HRGPs was also detected in the host cytoplasm. The aberrant distribution of HRGPs in infected cells of mutant-induced nodules likely reflects one aspect of the altered host metabolism in relation to peribacteroid-membrane breakdown. The possibility that the antiserum used for HRGP localization may have cross-reacted with ENOD 2 gene products is discussed in relation to amino-acid sequences and sites of accumulation. 相似文献
2.
Andreas F. Haag Silvia Wehmeier Sebastian Beck Victoria L. Marlow Vivien Fletcher Euan K. James Gail P. Ferguson 《Journal of bacteriology》2009,191(14):4681-4686
Free-living Sinorhizobium meliloti lpxXL and acpXL mutants lack lipid A very-long-chain fatty acids (VLCFAs) and have reduced competitiveness in alfalfa. We demonstrate that LpxXL and AcpXL play important but distinct roles in bacteroid development and that LpxXL is essential for the modification of S. meliloti bacteroid lipid A with VLCFAs.Sinorhizobium meliloti and Brucella abortus form chronic intracellular infections within legumes and mammalian hosts, respectively (3, 20), and their BacA proteins play essential roles in these processes (8, 12). The precise function(s) of the BacA proteins has not been resolved, but free-living S. meliloti and B. abortus mutants lacking BacA have increased resistance to the glycopeptide bleomycin (9, 12) and there are ∼50% decreases in their lipid A very-long-chain fatty acid (VLCFA) contents (4, 7). It has also been determined that the increased resistance of an S. meliloti bacA null mutant to bleomycin and a truncated eukaryotic peptide, Bac71-16, is independent of its lipid A VLCFA alteration (6, 15). Together, these findings support a model in which BacA could have multiple nonoverlapping functions which lead to lipid A VLCFA modification and peptide uptake. The fact that two symbiotically defective S. meliloti BacA site-directed mutants (Q193G and R389G) (13) show defects in BacA-mediated lipid A VLCFA modification (4) but are still capable of peptide uptake (15) suggests that the S. meliloti lipid A VLCFA modification could play a key role in the symbiosis of this organism with alfalfa.Since the mechanism by which BacA leads to the lipid A VLCFA modification has not been resolved (4), S. meliloti mutants were constructed with mutations in the lpxXL and acpXL genes, which encode a lipid A VLCFA acyl transferase and a VLCFA acyl carrier protein directly involved in the biosynthesis of VLCFA-modified lipid A (5, 23). The S. meliloti lpxXL and acpXL mutants completely lack the lipid A VLCFA modification in their free-living states, but, unlike the S. meliloti bacA null mutant, these mutants can still form a successful symbiosis with alfalfa (5, 8, 23). However, the fact that the S. meliloti acpXL and lpxXL mutants are substantially less competitive in the alfalfa symbiosis than the parent strain (5, 23) indicates that the AcpXL and LpxXL proteins play important roles in at least one of the stages of the alfalfa symbiosis. Although the free-living S. meliloti acpXL and lpxXL mutants completely lack the lipid A VLCFA, they produce different species of lipid A (5). For example, in the absence of AcpXL, S. meliloti is able to modify lipid A with either C16:0 or C18:0 in the position normally modified with the VLCFA in the parent strain lipid A. This process is LpxXL dependent, as it does not occur in either an S. meliloti lpxXL single mutant or an S. meliloti acpXL lpxXL double mutant. In addition, since a Rhizobium leguminosarum acpXL mutant completely lacks the lipid A VLCFA modification in its free-living state but its lipid A is partially modified with the VLCFA to ∼58% of the amount in the parent strain lipid A during passage through peas (25), it is also possible that the S. meliloti acpXL mutant and possibly the S. meliloti lpxXL mutant undergo further lipid A changes during the interaction with alfalfa.In this study, we found that LpxXL and AcpXL play important but distinct roles in S. meliloti bacteroid development during alfalfa symbiosis. Additionally, we demonstrated that there is a minor host-induced AcpXL-independent mechanism by which S. meliloti bacteroid lipopolysaccharide (LPS) can be modified with the VLCFA. In contrast, we found that the LpxXL protein plays an essential role in the modification of S. meliloti bacteroids with VLCFAs. 相似文献
3.
Microsporidia comprise a highly diverged phylum of intracellular, eukaryotic pathogens, with some species able to cause life-threatening illnesses in immunocompromised patients. To better understand microsporidian infection in animals, we study infection of the genetic model organism Caenorhabditis elegans and a species of microsporidia, Nematocida parisii, which infects Caenorhabditis nematodes in the wild. We conducted a targeted RNAi screen for host C. elegans genes important for infection and growth of N. parisii, using nematode larval arrest as an assay for infection. Here, we present the results of this RNAi screen, and our analyses on one of the RNAi hits from the screen that was ultimately not corroborated by loss of function mutants. This hit was an RNAi clone against F56A8.3, a conserved gene that encodes a transmembrane protein containing leucine-rich repeats (LRRs), a domain found in numerous pathogen receptors from other systems. This RNAi clone caused C. elegans to be resistant to infection by N. parisii, leading to reduced larval arrest and lower pathogen load. Characterization of the endogenous F56A8.3 protein revealed that it is expressed in the intestine, localized to the membrane around lysosome-related organelles (LROs), and exists in two different protein isoforms in C. elegans. We used the CRISPR-Cas9 system to edit the F56A8.3 locus and created both a frameshift mutant resulting in a truncated protein and a complete knockout mutant. Neither of these mutants was able to recapitulate the infection phenotypes of the RNAi clone, indicating that the RNAi-mediated phenotypes are due to an off-target effect of the RNAi clone. Nevertheless, this study describes microsporidia-induced developmental arrest in C. elegans, presents results from an RNAi screen for host genes important for microsporidian infection, and characterizes aspects of the conserved F56A8.3 gene and its protein product. 相似文献
4.
Christian Sohlenkamp Christian R.H. Raetz Brian O. Ingram 《Biochimica et Biophysica Acta (BBA)/Molecular and Cell Biology of Lipids》2013,1831(7):1250-1259
The lipid A component of lipopolysaccharide from the nitrogen-fixing plant endosymbiont, Rhizobium etli, is structurally very different from that found in most enteric bacteria. The lipid A from free-living R. etli is structurally heterogeneous and exists as a mixture of species which are either pentaacylated or tetraacylated. In contrast, the lipid A from R. etli bacteroids is reported to consist exclusively of tetraacylated lipid A species. The tetraacylated lipid A species in both cases lack a β-hydroxymyristoyl chain at the 3-position of lipid A. Here, we show that the lipid A modification enzyme responsible for 3-O deacylation in R. etli is a homolog of the PagL protein originally described in Salmonella enterica sv. typhimurium. In contrast to the PagL proteins described from other species, R. etli PagL displays a calcium dependency. To determine the importance of the lipid A modification catalyzed by PagL, we isolated and characterized a R. etli mutant deficient in the pagL gene. Mass spectrometric analysis confirmed that the mutant strain was exclusively tetraacylated and radiochemical analysis revealed that 3-O deacylase activity was absent in membranes prepared from the mutant. The R. etli mutant was not impaired in its ability to form nitrogen-fixing nodules on Phaseolus vulgaris but it displayed slower nodulation kinetics relative to the wild-type strain. The lipid A modification catalyzed by R. etli PagL, therefore, is not required for nodulation but may play other roles such as protecting bacterial endosymbionts from plant immune responses during infection. 相似文献
5.
Luis E. Servín-Garcidue?as Marco A. Rogel Ernesto Orme?o-Orrillo Alfonso Delgado-Salinas Julio Martínez-Romero Federico Sánchez Esperanza Martínez-Romero 《Journal of bacteriology》2012,194(22):6310-6311
We present the genome sequence of Rhizobium sp. strain CCGE510, a nitrogen fixing bacterium taxonomically affiliated with the R. leguminosarum-R. etli group, isolated from wild Phaseolus albescens nodules grown in native pine forests in western Mexico. P. albescens is an endangered bean species phylogenetically related to P. vulgaris. In spite of the close host relatedness, Rhizobium sp. CCGE510 does not establish an efficient symbiosis with P. vulgaris. This is the first genome of a Rhizobium symbiont from a Phaseolus species other than P. vulgaris, and it will provide valuable new insights about symbiont-host specificity. 相似文献
6.
7.
8.
Increased Bean (Phaseolus vulgaris L.) Nodulation Competitiveness of Genetically Modified Rhizobium Strains 总被引:6,自引:4,他引:2
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Rhizobium leguminosarum bv. phaseoli strain collections harbor heterogeneous groups of bacteria in which two main types of strains may be distinguished, differing both in the symbiotic plasmid and in the chromosome. We have analyzed under laboratory conditions the competitive abilities of the different types of Rhizobium strains capable of nodulating Phaseolus vulgaris L. bean. R. leguminosarum bv. phaseoli type I strains (characterized by nif gene reiterations and a narrow host range) are more competitive than type II strains (that have a broad host range), and both types are more competitive than the promiscuous rhizobia isolated from other tropical legumes able to nodulate beans. Type I strains become even more competitive by the transfer of a non-Sym, 225-kilobase plasmid from type II strain CFN299. This plasmid has been previously shown to enhance the nodulation and nitrogen fixation capabilities of Agrobacterium tumefaciens transconjugants carrying the Sym plasmid of strain CFN299. Other type I R. leguminosarum bv. phaseoli transconjugants carrying two symbiotic plasmids (type I and type II) have been constructed. These strains have a diminished competitive ability. The increase of competitiveness obtained in some transconjugants seems to be a transient property. 相似文献
9.
10.
Markus F. F. Arnold Paola Caro-Hernandez Karen Tan Giulia Runti Silvia Wehmeier Marco Scocchi William T. Doerrler Graham C. Walker Gail P. Ferguson 《Journal of bacteriology》2014,196(2):436-444
yaiW is a previously uncharacterized gene found in enteric bacteria that is of particular interest because it is located adjacent to the sbmA gene, whose bacA ortholog is required for Sinorhizobium meliloti symbiosis and Brucella abortus pathogenesis. We show that yaiW is cotranscribed with sbmA in Escherichia coli and Salmonella enterica serovar Typhi and Typhimurium strains. We present evidence that the YaiW is a palmitate-modified surface exposed outer membrane lipoprotein. Since BacA function affects the very-long-chain fatty acid (VLCFA) modification of S. meliloti and B. abortus lipid A, we tested whether SbmA function might affect either the fatty acid modification of the YaiW lipoprotein or the fatty acid modification of enteric lipid A but found that it did not. Interestingly, we did observe that E. coli SbmA suppresses deficiencies in the VLCFA modification of the lipopolysaccharide of an S. meliloti
bacA mutant despite the absence of VLCFA in E. coli. Finally, we found that both YaiW and SbmA positively affect the uptake of proline-rich Bac7 peptides, suggesting a possible connection between their cellular functions. 相似文献
11.
Autophagy has been shown to contribute to defense against intracellular
bacteria and parasites. In comparison, the ability of such pathogens to
manipulate host cell autophagy to their advantage has not been examined. Here
we present evidence that infection by Toxoplasma gondii, an
intracellular protozoan parasite, induces host cell autophagy in both HeLa
cells and primary fibroblasts, via a mechanism dependent on host Atg5 but
independent of host mammalian target of rapamycin suppression. Infection led
to the conversion of LC3 to the autophagosome-associated form LC3-II, to the
accumulation of LC3-containing vesicles near the parasitophorous vacuole, and
to the relocalization toward the vacuole of structures labeled by the
phosphatidylinositol 3-phosphate indicator YFP-2×FYVE. The autophagy
regulator beclin 1 was concentrated in the vicinity of the parasitophorous
vacuole in infected cells. Inhibitor studies indicated that parasite-induced
autophagy is dependent on calcium signaling and on abscisic acid. At
physiologically relevant amino acid levels, parasite growth became defective
in Atg5-deficient cells, indicating a role for host cell autophagy in parasite
recovery of host cell nutrients. A flow cytometric analysis of cell size as a
function of parasite content revealed that autophagy-dependent parasite growth
correlates with autophagy-dependent consumption of host cell mass that is
dependent on parasite progression. These findings indicate a new role for
autophagy as a pathway by which parasites may effectively compete with the
host cell for limiting anabolic resources.Macroautophagy (hereafter referred to as autophagy) is a major catabolic
process in which cytosolic constituents are sequestered within
double-membraned vesicles (autophagosomes) and subsequently delivered to
lysosomes for degradation. Current evidence indicates at least two distinct
functions for this process. On the one hand, autophagy can be up-regulated
under nutrient-limiting conditions to increase nutrient supply via recycling
of the products of autophagic degradation, which may be exported from the
lysosome (1). The up-regulation
of autophagy upon starvation is thought to be mediated by the suppression of
signaling through the mTOR pathway
(2). On the other hand,
autophagy can serve to maintain cellular homeostasis by facilitating the
removal of damaged or deleterious elements, such as misfolded protein
aggregates (3). An important
example of the latter function is the role of autophagy in restricting the
growth of intracellular pathogens, including both free bacteria that have
escaped into host cytosol, such as group A Streptococcus, and
pathogens, such as Mycobacterium tuberculosis, that reside in
parasitophorous vacuoles in macrophages
(4,
5). In macrophages infected
with Toxoplasma gondii, fusion of the parasitophorous vacuole with
lysosomes can be induced in an autophagy-dependent manner when host cell
anti-parasitic function is activated via CD40
(6). Autophagy as a component
of host defense may be up-regulated by inflammatory agents such as
lipopolysaccharide (7) and
interferon-γ (8).Although the clearance function of autophagy may enhance pathogen killing
in host cells that have been activated to generate antimicrobial or
antiparasitic function, in permissive host cells, in which the pathogen is
less susceptible to sequestration by the autophagosome, autophagy may
conceivably play a quite different role. Modulation of the balance between
anabolic and catabolic processes may affect the outcome of competition between
pathogen and host cell for limiting nutrients. In particular, the nutritive
function of autophagy could favor pathogen expansion by providing greater
access to host cell biomass. The intracellular apicomplexan parasite, T.
gondii, is a suitable agent for the investigation of this hypothesis,
because it has been shown to be highly dependent on its host cell for the
supply of several nutrients, including amino acids
(9), lipids
(10), and purines
(11). T. gondii
replicates within a parasitophorous vacuole that, in permissive host cells, is
protected from lysosomal fusion. Recent evidence indicates that in such
permissive cells, in which the parasite can differentiate into bradyzoites
associated with chronic infection, the pathogen is able to actively sequester
host cell lysosome-derived vesicles, thereby potentially gaining access to
their contents (12).The ability of intracellular parasites to regulate host cell autophagy has
been little examined, and there is also little information with respect to the
impact of these pathogens on host cell signals that potentially affect the
autophagic pathway. In addition to mTOR, these include calcium ions, which
have been implicated in autophagy induced by endoplasmic reticulum stress
(13). In this study, we
provide evidence that T. gondii induces host cell autophagy by a
mechanism dependent on calcium but independent of mTOR and that it exploits
the nutritive function of host autophagy to enhance its proliferation. 相似文献
12.
Prevalence of the Rhizobium etli-Like Allele in Genes Coding for 16S rRNA among the Indigenous Rhizobial Populations Found Associated with Wild Beans from the Southern Andes in Argentina
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O. Mario Aguilar María Vernica Lpez Pablo M. Riccillo Ramn A. Gonzlez Marcela Pagano Daniel H. Grasso Alfred Pühler Gabriel Favelukes 《Applied microbiology》1998,64(9):3520-3524
A collection of rhizobial isolates from nodules of wild beans, Phaseolus vulgaris var. aborigineus, found growing in virgin lands in 17 geographically separate sites in northwest Argentina was characterized on the basis of host range, growth, hybridization to a nifH probe, analysis of genes coding for 16S rRNA (16S rDNA), DNA fingerprinting, and plasmid profiles. Nodules in field-collected wild bean plants were largely dominated by rhizobia carrying the 16S rDNA allele of Rhizobium etli. A similar prevalence of the R. etli allele was observed among rhizobia trapped from nearby soil. Intragroup diversity of wild bean isolates with either R. etli-like or Rhizobium leguminosarum bv. phaseoli-like alleles was generally found across northwest Argentina. The predominance of the R. etli allele suggests that in this center of origin of P. vulgaris the coevolution of Rhizobium spp. and primitive beans has resulted in this preferential symbiotic association. 相似文献
13.
Different species and symbiotic genotypes of field rhizobia can nodulate Phaseolus vulgaris in Tunisian soils 总被引:4,自引:0,他引:4
Ridha Mhamdi Gisèle Laguerre Mohamed Elarbi Aouani Mohamed Mars Noëlle Amarger 《FEMS microbiology ecology》2002,41(1):77-84
A collection of 160 isolates of rhizobia nodulating Phaseolus vulgaris in three geographical regions in Tunisia was characterized by restriction fragment length polymorphism analysis of polymerase chain reaction (PCR)-amplified 16S rDNA, nifH and nodC genes. Nine groups of rhizobia were delineated: Rhizobium gallicum biovar (bv.) gallicum, Rhizobium leguminosarum bv. phaseoli and bv. viciae, Rhizobium etli bv. phaseoli, Rhizobium giardinii bv. giardinii, and four groups related to species of the genus Sinorhizobium, Sinorhizobium meliloti, Sinorhizobium medicae and Sinorhizobium fredii. The most abundant rhizobial species were R. gallicum, R. etli, and R. leguminosarum encompassing 29–20% of the isolates each. Among the isolates assigned to R. leguminosarum, two-thirds were ineffective in nitrogen fixation with P. vulgaris and harbored a symbiotic gene typical of the biovar viciae. The S. fredii-like isolates did not nodulate soybean plants but formed numerous effective nodules on P. vulgaris. Comparison of nodC gene sequences showed that their symbiotic genotype was not related to that of S. fredii, but to that of the S. fredii-like reference strain GR-06, which was isolated from a bean plant grown in a Spanish soil. An additional genotype including 16% of isolates was found to be closely related to species of the genus Agrobacterium. However, when re-examined, these isolates did not nodulate their original host. 相似文献
14.
Claudine Belon Chantal Soscia Audrey Bernut Aurélie Laubier Sophie Bleves Anne-Béatrice Blanc-Potard 《PLoS pathogens》2015,11(6)
Pathogenic bacteria have developed strategies to adapt to host environment and resist host immune response. Several intracellular bacterial pathogens, including Salmonella enterica and Mycobacterium tuberculosis, share the horizontally-acquired MgtC virulence factor that is important for multiplication inside macrophages. MgtC is also found in pathogenic Pseudomonas species. Here we investigate for the first time the role of MgtC in the virulence of an extracellular pathogen, Pseudomonas aeruginosa. A P. aeruginosa mgtC mutant is attenuated in the systemic infection model of zebrafish embryos, and strikingly, the attenuated phenotype is dependent on the presence of macrophages. In ex vivo experiments, the P. aeruginosa mgtC mutant is more sensitive to macrophage killing than the wild-type strain. However, wild-type and mutant strains behave similarly toward macrophage killing when macrophages are treated with an inhibitor of the vacuolar proton ATPase. Importantly, P. aeruginosa mgtC gene expression is strongly induced within macrophages and phagosome acidification contributes to an optimal expression of the gene. Thus, our results support the implication of a macrophage intracellular stage during P. aeruginosa acute infection and suggest that Pseudomonas MgtC requires phagosome acidification to play its intracellular role. Moreover, we demonstrate that P. aeruginosa MgtC is required for optimal growth in Mg2+ deprived medium, a property shared by MgtC factors from intracellular pathogens and, under Mg2+ limitation, P. aeruginosa MgtC prevents biofilm formation. We propose that MgtC shares a similar function in intracellular and extracellular pathogens, which contributes to macrophage resistance and fine-tune adaptation to host immune response in relation to the different bacterial lifestyles. In addition, the phenotypes observed with the mgtC mutant in infection models can be mimicked in wild-type P. aeruginosa strain by producing a MgtC antagonistic peptide, thus highlighting MgtC as a promising new target for anti-virulence strategies. 相似文献
15.
16.
Marta C. Nunes Mami Okada Christine Scheidig-Benatar Brian M. Cooke Artur Scherf 《PloS one》2010,5(7)
Background
Modulation of infected host cells by intracellular pathogens is a prerequisite for successful establishment of infection. In the human malaria parasite Plasmodium falciparum, potential candidates for erythrocyte remodelling include the apicomplexan-specific FIKK kinase family (20 members), several of which have been demonstrated to be transported into the erythrocyte cytoplasm via Maurer''s clefts.Methodology
In the current work, we have knocked out two members of this gene family (Pf fikk7.1 and Pf fikk12), whose products are localized at the inner face of the erythrocyte membrane. Both mutant parasite lines were viable and erythrocytes infected with these parasites showed no detectable alteration in their ability to adhere in vitro to endothelial receptors such as chondroitin sulfate A and CD36. However, we observed sizeable decreases in the rigidity of infected erythrocytes in both knockout lines. Mutant parasites were further analyzed using a phospho-proteomic approach, which revealed distinct phosphorylation profiles in ghost preparations of infected erythrocytes. Knockout parasites showed a significant reduction in the level of phosphorylation of a protein of approximately 80 kDa for FIKK12-KO in trophozoite stage and a large protein of about 300 kDa for FIKK7.1-KO in schizont stage.Conclusions
Our results suggest that FIKK members phosphorylate different membrane skeleton proteins of the infected erythrocyte in a stage-specific manner, inducing alterations in the mechanical properties of the parasite-infected red blood cell. This suggests that these host cell modifications may contribute to the parasites'' survival in the circulation of the human host. 相似文献17.
Judith A. Smith Mike Khan Diogo D. Magnani Jerome S. Harms Marina Durward Girish K. Radhakrishnan Yi-Ping Liu Gary A. Splitter 《PLoS pathogens》2013,9(12)
Brucella melitensis is a facultative intracellular bacterium that causes brucellosis, the most prevalent zoonosis worldwide. The Brucella intracellular replicative niche in macrophages and dendritic cells thwarts immune surveillance and complicates both therapy and vaccine development. Currently, host-pathogen interactions supporting Brucella replication are poorly understood. Brucella fuses with the endoplasmic reticulum (ER) to replicate, resulting in dramatic restructuring of the ER. This ER disruption raises the possibility that Brucella provokes an ER stress response called the Unfolded Protein Response (UPR). In this study, B. melitensis infection up regulated expression of the UPR target genes BiP, CHOP, and ERdj4, and induced XBP1 mRNA splicing in murine macrophages. These data implicate activation of all 3 major signaling pathways of the UPR. Consistent with previous reports, XBP1 mRNA splicing was largely MyD88-dependent. However, up regulation of CHOP, and ERdj4 was completely MyD88 independent. Heat killed Brucella stimulated significantly less BiP, CHOP, and ERdj4 expression, but induced XBP1 splicing. Although a Brucella VirB mutant showed relatively intact UPR induction, a TcpB mutant had significantly compromised BiP, CHOP and ERdj4 expression. Purified TcpB, a protein recently identified to modulate microtubules in a manner similar to paclitaxel, also induced UPR target gene expression and resulted in dramatic restructuring of the ER. In contrast, infection with the TcpB mutant resulted in much less ER structural disruption. Finally, tauroursodeoxycholic acid, a pharmacologic chaperone that ameliorates the UPR, significantly impaired Brucella replication in macrophages. Together, these results suggest Brucella induces a UPR, via TcpB and potentially other factors, that enables its intracellular replication. Thus, the UPR may provide a novel therapeutic target for the treatment of brucellosis. These results also have implications for other intracellular bacteria that rely on host physiologic stress responses for replication. 相似文献
18.
Manganese transport is essential for N2‐fixation by Rhizobium leguminosarum in bacteroids from galegoid but not phaseoloid nodules
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Graham Hood Vinoy Ramachandran Alison K. East J. Allan Downie Philip S. Poole 《Environmental microbiology》2017,19(7):2715-2726
Rhizobium leguminosarum has two high‐affinity Mn2+ transport systems encoded by sitABCD and mntH. In symbiosis, sitABCD and mntH were expressed throughout nodules and also strongly induced in Mn2+‐limited cultures of free‐living cells. Growth of a sitA mntH double mutant was severely reduced under Mn2+ limitation and sitA and mntH single mutants were more sensitive to oxidative stress. The double sitA mntH mutant of R. leguminosarum was unable to fix nitrogen (Fix‐) with legumes belonging to the galegoid clade (Pisum sativum, Vicia faba and Vicia hirsuta). The presence of infection thread‐like structures and sparsely‐packed plant cells in nodules suggest that bacteroid development was blocked, either at a late stage of infection thread progression or during bacteroid‐release. In contrast, a double sitA mntH mutant was Fix+ on common bean (Phaseoli vulgaris), a member of the phaseoloid clade of legumes, indicating a host‐specific symbiotic requirement for Mn2+ transport. 相似文献
19.
Laura Azeredo Miranda Mota Jo?o Roberto Neto Ver?nica Gomes Monteiro Caroliny Samary Silva Lobato Marco Antonio de Oliveira Maura da Cunha Heloisa D’ávila Sérgio Henrique Seabra Patrícia Torres Bozza Renato Augusto DaMatta 《Memórias do Instituto Oswaldo Cruz》2014,109(6):767-774
Lipid bodies [lipid droplets (LBs)] are lipid-rich organelles involved in lipid
metabolism, signalling and inflammation. Recent findings suggest a role for LBs in
host response to infection; however, the potential functions of this organelle
in Toxoplasma gondii infection and how it alters macrophage
microbicidal capacity during infection are not well understood. Here, we investigated
the role of host LBs in T. gondii infection in mouse peritoneal
macrophages in vitro. Macrophages cultured with mouse serum (MS) had higher numbers
of LBs than those cultured in foetal bovine serum and can function as a model to
study the role of LBs during intracellular pathogen infection. LBs were found in
association with the parasitophorous vacuole, suggesting that T. gondii
may benefit from this lipid source. Moreover, increased numbers of
macrophage LBs correlated with high prostaglandin E2 (PGE2) production and decreased
nitric oxide (NO) synthesis. Accordingly, LB-enriched macrophages cultured with MS
were less efficient at controlling T. gondii growth. Treatment of
macrophages cultured with MS with indomethacin, an inhibitor of PGE2 production,
increased the microbicidal capacity against T. gondii. Collectively,
these results suggest that culture with MS caused a decrease in microbicidal activity
of macrophages against T. gondii by increasing PGE2 while lowering
NO production. 相似文献
20.
Mohamed Hashem Eman S. H. Farrag 《Archives Of Phytopathology And Plant Protection》2013,46(7):676-687
Abstract Tobacco necrosis virus (TNV) was tested to induce systemic acquired resistance (SAR) in Phaseolus vulgaris cv. Lima against three important soil-borne fungal pathogens viz: Rhizoctonia solani, Macrophomina phaseolina and Fusarium oxysporum. Application of TNV as a local infection of seven-day old primary leaves of Phaseolus vulgaris cv. Lima resulted in reduction of the mean disease rating of root-rot and damping-off caused by the tested fungal pathogens. The pre-inoculated plants with TNV showed a significant enhancement in their content of photosynthetic pigments (chlorophyll a, b and carotenoids) compared to those inoculated with fungal pathogens only. The percentage of cell membrane stability and ion leakage of viral-treated plants were significantly increased confirming the healthy cytological status of the treated plants. Results demonstrated that inoculation of the primary leaves of beans with TNV before infection with the fungal pathogens leads to changes in protein patterns and showed differences compared with control and caused the appearance of at least one new protein band compared with only fungal-infected plants. Also, an increase in peroxidase activity emerged in the thickness of the isozymic pattern in addition to the synthesis of new bands which was observed as a result of TNV application before infection with the three fungal pathogens. Induction of the synthesis of a new protein and increasing peroxidase activity in the inoculated plants enhanced the defense system against the target pathogen. The results greatly supported the successful application of TNV in the induction of systemic acquired resistance in P. vulgaris cv. Lima against the fungal pathogens. 相似文献