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The receiver domain of hybrid histidine kinase VirA: an enhancing factor for vir gene expression in Agrobacterium tumefaciens.
J Bacteriol. 2010 Mar; 192(6):1534-42.JB

Abstract

The plant pathogen Agrobacterium tumefaciens expresses virulence (vir) genes in response to chemical signals found at the site of a plant wound. VirA, a hybrid histidine kinase, and its cognate response regulator, VirG, regulate vir gene expression. The receiver domain at the carboxyl end of VirA has been described as an inhibitory element because its removal increased vir gene expression relative to that of full-length VirA. However, experiments that characterized the receiver region as an inhibitory element were performed in the presence of constitutively expressed virG. We show here that VirA's receiver domain is an activating factor if virG is expressed from its native promoter on the Ti plasmid. When virADeltaR was expressed from a multicopy plasmid, both sugar and the phenolic inducer were essential for vir gene expression. Replacement of wild-type virA on pTi with virADeltaR precluded vir gene induction, and the cells did not accumulate VirG or induce transcription of a virG-lacZ fusion in response to acetosyringone. These phenotypes were corrected if the virG copy number was increased. In addition, we show that the VirA receiver domain can interact with the VirG DNA-binding domain.

Authors+Show Affiliations

Department of Biology, University of Pennsylvania, Philadelphia, PA 19104-6018, USA. wisea2@sas.upenn.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

20081031

Citation

Wise, Arlene A., et al. "The Receiver Domain of Hybrid Histidine Kinase VirA: an Enhancing Factor for Vir Gene Expression in Agrobacterium Tumefaciens." Journal of Bacteriology, vol. 192, no. 6, 2010, pp. 1534-42.
Wise AA, Fang F, Lin YH, et al. The receiver domain of hybrid histidine kinase VirA: an enhancing factor for vir gene expression in Agrobacterium tumefaciens. J Bacteriol. 2010;192(6):1534-42.
Wise, A. A., Fang, F., Lin, Y. H., He, F., Lynn, D. G., & Binns, A. N. (2010). The receiver domain of hybrid histidine kinase VirA: an enhancing factor for vir gene expression in Agrobacterium tumefaciens. Journal of Bacteriology, 192(6), 1534-42. https://doi.org/10.1128/JB.01007-09
Wise AA, et al. The Receiver Domain of Hybrid Histidine Kinase VirA: an Enhancing Factor for Vir Gene Expression in Agrobacterium Tumefaciens. J Bacteriol. 2010;192(6):1534-42. PubMed PMID: 20081031.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The receiver domain of hybrid histidine kinase VirA: an enhancing factor for vir gene expression in Agrobacterium tumefaciens. AU - Wise,Arlene A, AU - Fang,Fang, AU - Lin,Yi-Han, AU - He,Fanglian, AU - Lynn,David G, AU - Binns,Andrew N, Y1 - 2010/01/15/ PY - 2010/1/19/entrez PY - 2010/1/19/pubmed PY - 2010/4/16/medline SP - 1534 EP - 42 JF - Journal of bacteriology JO - J. Bacteriol. VL - 192 IS - 6 N2 - The plant pathogen Agrobacterium tumefaciens expresses virulence (vir) genes in response to chemical signals found at the site of a plant wound. VirA, a hybrid histidine kinase, and its cognate response regulator, VirG, regulate vir gene expression. The receiver domain at the carboxyl end of VirA has been described as an inhibitory element because its removal increased vir gene expression relative to that of full-length VirA. However, experiments that characterized the receiver region as an inhibitory element were performed in the presence of constitutively expressed virG. We show here that VirA's receiver domain is an activating factor if virG is expressed from its native promoter on the Ti plasmid. When virADeltaR was expressed from a multicopy plasmid, both sugar and the phenolic inducer were essential for vir gene expression. Replacement of wild-type virA on pTi with virADeltaR precluded vir gene induction, and the cells did not accumulate VirG or induce transcription of a virG-lacZ fusion in response to acetosyringone. These phenotypes were corrected if the virG copy number was increased. In addition, we show that the VirA receiver domain can interact with the VirG DNA-binding domain. SN - 1098-5530 UR - https://www.unboundmedicine.com/medline/citation/20081031/The_receiver_domain_of_hybrid_histidine_kinase_VirA:_an_enhancing_factor_for_vir_gene_expression_in_Agrobacterium_tumefaciens_ L2 - http://jb.asm.org/cgi/pmidlookup?view=long&pmid=20081031 DB - PRIME DP - Unbound Medicine ER -