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pubmed-article:7961454pubmed:abstractTextThe phototaxis-deficient mutant of Halobacterium salinarium, Pho81, lacks both sensory rhodopsin I (SR-I) and its putative transducer protein HtrI, according to immunoblotting and spectroscopic criteria. From restriction analysis and selected DNA sequencing, we have determined that the SR-I- HtrI- phenotype results from an insertion of a 520-bp transposable element, ISH2, into the coding region of the SR-I apoprotein gene sopI and deletion of 11 kbp upstream of ISH2 including the first 164 bp of sopI and the entire htrI gene. SR-I and HtrI expression as well as full phototaxis sensitivity are restored by transformation with a halobacterial plasmid carrying the htrI-sopI gene pair and their upstream promoter region. An internal deletion of a portion of htrI encoding the putative methylation and signaling domains of HtrI (253 residues) prevents the restoration of phototaxis, providing further evidence for the role of HtrI as a transducer for SR-I. Analysis of flash-induced photochemical reactions of SR-I over a range of pH shows that the partially deleted HtrI maintains SR-I interactions sites responsible for modulation of the SR-I photocycle.lld:pubmed
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pubmed-article:7961454pubmed:articleTitleIdentification of distinct domains for signaling and receptor interaction of the sensory rhodopsin I transducer, HtrI.lld:pubmed
pubmed-article:7961454pubmed:affiliationDepartment of Microbiology and Molecular Genetics, University of Texas Medical School Health Science Center, Houston 77030.lld:pubmed
pubmed-article:7961454pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7961454pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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