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bvrS from Brucella melitensis bv. 1 str. 16M

Victor ID 1323
Gene Name bvrS from Brucella melitensis bv. 1 str. 16M
Sequence Strain (Species/Organism) Brucella melitensis bv. 1 str. 16M
NCBI Gene ID 1197746
NCBI Protein GI 17988318
Locus Tag BMEI2035
Protein Accession NP_540952.1
Other Database IDs UniProtKB-ID: D0B3Y0_BRUME
UniRef100: UniRef100_D0B3Y0
UniRef90: UniRef90_A6WX45
UniRef50: UniRef50_Q07737
UniParc: UPI00000582D6
EMBL: GG703778
EMBL-CDS: EEW88104.1
RefSeq_NT: NC_003317.1
OMA: ILYLNQF
Taxonomy ID 224914
Chromosome No I
Gene Starting Position 2095498
Gene Ending Position 2097303
Gene Strand (Orientation) -
Protein Name SENSOR PROTEIN CHVG
DNA Sequence
>gi|17986284:2095498-2097303 Brucella melitensis bv. 1 str. 16M chromosome chromosome I, complete sequence
GTCATGCGCTGGCCGGAAGATCAACGATAAAGCGGGCACCCTTGAAAATATCCGGCTTATCCGGATCGGT
AATATTTTCCGCCGTCAGCGTGCCGCCATGCGCCTCGATGATCTGCCGGCTGATCGACAGGCCGAGGCCG
GAATTCTGCCCGAATGCTTCCGATGCCGGGCGATCCGTGTAGAAACGCTCGAAGATGCGCTCGATATTCT
CGATAGGAATGCCGGGGCCGTTATCCTCGACCAGAATGCGCAGCCGGTTGCCTTCGCCGGCCAGCGTAAC
GACGATACGGCCCGTATCGTCAGGCACGAAGGAGCGCGCATTCTCGATAAGGTTGCTTACCACCTGCCCA
AGACGCAGATCGTGGCCGGCGACATAGAAGCCTTTCTTGCCGGTGGGCAGCTTGCCCGTGTTGAACACGA
TTTCGGTGCCGACCTTGTTGCGCCGCACTTCGCGGGCGGCAGTCACAAGGCTGGTGAGAAGCTTTTTCAT
ATCCACGCGGTCGATATGTTCGCGCGCAAGCTCGGCATCGAGGCGCGAAGCGTCGGAAATATCCGTGATA
AGGCGGTCCAGCCGCCGCACGTCGTGCTGGATGACATCGAGCAGGCGCTTGCGTGATTCGTCGGTCTTGG
CGAGCGGCAGGGTTTCGACTGCGCTGCGAAGCGAGGTGAGGGGGTTCTTCAGCTCATGGCTGACATCGGC
TGCGAAGCTTTCAATGGCTTCGATGCGCGTATAAAGCGCGTCCGTCATGTCGCGGATGGAGGTGGAAAGG
TGGCCCACCTCGTCCTGACGCTCGGAAAAATCGGGAATTTCCACGCGGTTTTTCACGCCATGGCGCACCC
GGTCCGCCGCAGCCGAAAGCTTGCGCAAGGGGTTGGCAATTGTTGAGGCGAGGAAAAGCGACAGGATGAC
CATGACCGCCGACACAACGCCGAACACGCGGAAAACCGCCATACGCTCGGCCTGAACGATCTTGTCGATA
TCATCGCCTTCGGTAGAAAGAAGCAGAACACCCAAAATGGCACGGGAGCGCTGGATAGGAACGGCCACGG
AAACGATCAGCTCACCGCGCTGATTGCGGCGCTGTGCCATCTGCGGCGAGCCGCTCAGCGCCTTGACGAT
TTCCTGATAGGCAAGGCCGTTTCCGCCCGGCTGCTCCTGGTAGAGCGGCAGGCCACCGCCATAGAAAAGG
CGCGACAGCCAGCTGCCGATACGTTCCCAAAGGGCAGGCGTCTCATCCTCTATCGGCGGCAGGTCATAGC
GCAGGACCGGCCCGCTGGACGGGAAGCTTGTCGAATAAAGCGCGCGCGAATCAAGCAGCTTATTCGCATA
GCGGTCATAGATGCGCGCGCGCGTGCTGGTCGGAGAGATCAACTGGCGCAGCAGCGGCGAAACCTTTTCG
GGATTGATCGGAAATTCCCAATTATCCGGCGAATCGGGGGAGGGGGTTATGCTCTGCCCGGCCTGAAGCT
CCAGAAGCTTTTCAGGGTCGATCAGCAGCGAATTGGTATCGACCGTAACCGATGCAGAAATCGCAGCAGC
GATGATCTTGCCCTGCGTCAGCAGGCTTTCGATCTTGGCGTCGATCAGCCCCTCGCGGAACTGGTTCATA
TAAAGAATGCCGGAAACCAGAACGGCCAGTGCTGCCAGGTTGAGAAACAGGATGCGGCGCGTCAGGCTTG
AAAAGAGATATTGCCCAAGAAACTTGCGCAAGGGCGACAGAAAGCGGCGCAGAAACACCGAGCGTTGCCG
CCGTGCTCTGCGCTCGCGCATCCCCGAAAGGCTATCTTTCTGGGTCTCTGCGACCA
Protein Sequence
>gi|17988318|ref|NP_540952.1| sensor protein CHVG [Brucella melitensis bv. 1 str. 16M] MVAETQKDSLSGMRERRARRQRSVFLRRFLSPLRKFLGQYLFSSLTRRILFLNLAALAVLVSGILYMNQFREGLIDAKIESLLTQGKIIAAAISASVTVDTNSLLIDPEKLLELQAGQSITPSPDSPDNWEFPINPEKVSPLLRQLISPTSTRARIYDRYANKLLDSRALYSTSFPSSGPVLRYDLPPIEDETPALWERIGSWLSRLFYGGGLPLYQEQPGGNGLAYQEIVKALSGSPQMAQRRNQRGELIVSVAVPIQRSRAILGVLLLSTEGDDIDKIVQAERMAVFRVFGVVSAVMVILSLFLASTIANPLRKLSAAADRVRHGVKNRVEIPDFSERQDEVGHLSTSIRDMTDALYTRIEAIESFAADVSHELKNPLTSLRSAVETLPLAKTDESRKRLLDVIQHDVRRLDRLITDISDASRLDAELAREHIDRVDMKKLLTSLVTAAREVRRNKVGTEIVFNTGKLPTGKKGFYVAGHDLRLGQVVSNLIENARSFVPDDTGRIVVTLAGEGNRLRILVEDNGPGIPIENIERIFERFYTDRPASEAFGQNSGLGLSISRQIIEAHGGTLTAENITDPDKPDIFKGARFIVDLPASA
Molecule Role Virulence factor
Molecule Role Annotation MUTATION: The two-component BvrSBvrR system is essential for Brucella abortus virulence. Disruption of BvrSBvrR damages the outer membrane, thus contributing to the severe attenuation manifested by bvrS and bvrR mutants. The bvrS and bvrR mutants are avirulent in mice, show reduced invasiveness to epithelial cells and macrophages, and are incapable of inhibiting lysosome fusion and replicating intracellularly (Manterola et al., 2005).

Mutations in the bvrR or bvrS genes hamper the penetration of B abortus in non-phagocytic cells and impairs intracellular trafficking and virulence. BvrRBvrS mutants do not recruit small GTPases of the Rho subfamily required for actin polymerization and penetration to cells. Dysfunction of the BvrRBvrS system alters the outer membrane permeability, the expression of several group 3 outer membrane proteins and the pattern of lipid A acylation. Constructs of virulent B abortus chimeras containing heterologous LPS from the bvrS(-) mutant demonstrated an altered permeability to cationic peptides similar to that of the BvrRBvrS mutants. It is hypothesized that the Brucella BvrRBvrS is a system devoted to the homeostasis of the outer membrane and, therefore in the interface for cell invasion and mounting the required structures for intracellular parasitism (López-Goñi et al., 2002).

In contrast to S2308 and S19, bvrS and bvrR mutant strains poorly invade HeLa cells and are rapidly targeted to cathepsin D- containing compartments (Pizarro-Cerdá et al., 1998).

B abortus bvrS bvrR mutants display reduced invasiveness and virulence (Briones et al., 2001).

Brucella bvrS and bvrR null mutants are defective in several outer membrane proteins, mainly Omp3a (former Omp25) and Omp3b as well as in the structure of the LPS molecule, but the O chain seems to be intact (Gorvel and Moreno, 2002).

Because bvrR and bvrS mutants are also altered in cell-surface hydrophobicity, permeability, and sensitivity to surface- targeted bactericidal peptides, it is proposed that BvrRBvrS controls cell envelope changes necessary to transit between extracellular and intracellular environments (Guzman-Verri et al., 2002).

BvrR/BvrS mutants are avirulent in mice, show reduced invasiveness in cells, and are unable to inhibit lysosome fusion and to replicate intracellularly (Guzman-Verri et al., 2002).
COG COG0642T, under T: Signal transduction mechanisms
References
Briones et al., 2001: Briones G, Iñón de Iannino N, Roset M, Vigliocco A, Paulo PS, Ugalde RA. Brucella abortus cyclic beta-1,2-glucan mutants have reduced virulence in mice and are defective in intracellular replication in HeLa cells. Infection and immunity. 2001; 69(7); 4528-4535. [PubMed: 11401996].
Gorvel and Moreno, 2002: Gorvel JP, Moreno E. Brucella intracellular life: from invasion to intracellular replication. Veterinary microbiology. 2002; 90(1-4); 281-297. [PubMed: 12414149].
Guzman-Verri et al., 2002: Guzman-Verri C, Manterola L, Sola-Landa A, Parra A, Cloeckaert A, Garin J, Gorvel JP, Moriyon I, Moreno E, Lopez-Goni I. The two-component system BvrR/BvrS essential for Brucella abortus virulence regulates the expression of outer membrane proteins with counterparts in members of the Rhizobiaceae. Proceedings of the National Academy of Sciences of the United States of America. 2002; 99(19); 12375-12380. [PubMed: 12218183].
López-Goñi et al., 2002: López-Goñi I, Guzmán-Verri C, Manterola L, Sola-Landa A, Moriyón I, Moreno E. Regulation of Brucella virulence by the two-component system BvrR/BvrS. Veterinary microbiology. 2002; 90(1-4); 329-339. [PubMed: 12414153].
Manterola et al., 2005: Manterola L, Moriyón I, Moreno E, Sola-Landa A, Weiss DS, Koch MH, Howe J, Brandenburg K, López-Goñi I. The lipopolysaccharide of Brucella abortus BvrS/BvrR mutants contains lipid A modifications and has higher affinity for bactericidal cationic peptides. Journal of bacteriology. 2005; 187(16); 5631-5639. [PubMed: 16077108].
Pizarro-Cerdá et al., 1998: Pizarro-Cerdá J, Méresse S, Parton RG, van der Goot G, Sola-Landa A, Lopez-Goñi I, Moreno E, Gorvel JP. Brucella abortus transits through the autophagic pathway and replicates in the endoplasmic reticulum of nonprofessional phagocytes. Infection and immunity. 1998; 66(12); 5711-5724. [PubMed: 9826346].